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Volume 24,Issue 8,2017 Table of Contents
2017, 24(8):815-827.
DOI: 10.3872/j.issn.1007-385X.2017.08.001
Abstract:
Genome-editing technologies that enable precise and stable modification of the genome are sparking a revolution in life science research and disease management. The discovery of the CRISPR/Cas9 technology repre-sents a huge breakthrough in the field of genome editing due to its easy operation and high efficiency, empowering scientists to manipulate genome editing to a broader extension. In this review, the classification of genome-editing technologies, the potential applications of the CRISPR/Cas9 system (including gene knockout, knock-in, methods of delivering CRISPR/Cas9 into cells, enhancing specificity of the CRISPR/Cas9, and accurate regulation of the CRIS-PR/Cas9) as well as broader applications of the CRISPR/Cas9 system (including base replacement, epigenetic regu-lation, regulation of endogenous gene expression, and genome-wide genetic screening) will be elaborated, respec-tively. Moreover, CRISPR/Cas9 in the field of cancer research, including generation of mouse models of cancer, gen-eration of cancer models of chromosome rearrangement, high-throughput screening of genes associated with tumor metastasis, as well as treatment of cancer will also be illustrated, providing readers with a general understanding of the CRISPR/Cas9 technology.
Genome-editing technologies that enable precise and stable modification of the genome are sparking a revolution in life science research and disease management. The discovery of the CRISPR/Cas9 technology repre-sents a huge breakthrough in the field of genome editing due to its easy operation and high efficiency, empowering scientists to manipulate genome editing to a broader extension. In this review, the classification of genome-editing technologies, the potential applications of the CRISPR/Cas9 system (including gene knockout, knock-in, methods of delivering CRISPR/Cas9 into cells, enhancing specificity of the CRISPR/Cas9, and accurate regulation of the CRIS-PR/Cas9) as well as broader applications of the CRISPR/Cas9 system (including base replacement, epigenetic regu-lation, regulation of endogenous gene expression, and genome-wide genetic screening) will be elaborated, respec-tively. Moreover, CRISPR/Cas9 in the field of cancer research, including generation of mouse models of cancer, gen-eration of cancer models of chromosome rearrangement, high-throughput screening of genes associated with tumor metastasis, as well as treatment of cancer will also be illustrated, providing readers with a general understanding of the CRISPR/Cas9 technology.
LI Huan
,
WANG Jiying
,
YU Pei
,
CHEN Shuying
,
XING Haiyan
,
TIAN Zheng
,
TANG Kejing
,
WANG Min
,
RAO Qing
2017, 24(8):828-832.
DOI: 10.3872/j.issn.1007-385X.2017.08.002
Abstract:
Objective: To determine the role of Rac1 GTPase activation in the regulation of leukemia cell quies-cence and investigate the possible mechanism. Methods: Constitutively active Rac1 lenti-virus vector was construct-ed to transfect KG-1a leukemia cells (Rac1-V12-KG-1a). The G0 phase cell ratio in sorted Rac1-V12-KG-1a and KG-1a cells transfected with empty vector (pCDH-KG-1a) was compared. Furthermore, after 4 days treatment with NSC23766, the Rac1-specific inhibitor, the G0 phase cell ratio in KG-1a cells was also detected. The expression lev-els of cell quiescence and cell cycle associated moleculars were then determined by RT-PCR. The G0 phase cell ra-tio of MPL - and MPL + leukemia cells in AML1-ETO9a leukemia mouse was detected by flow cytometry. Results:The results showed that the G0 phase cell ratio in Rac1-V12-KG-1a cells was significantly higher than that in pCDH-KG-1a cells ([15.30±0.60]% vs [11.50 ± 0.17]%, P<0.05). After the treatment of Rac1-specific inhibitor, the G0 phase cell ratio of the KG-1a cells was decreased significantly (P<0.05), and the effect was concentration depen-dent. RT-PCR showed that mRNA transcription levels of cell cycle related factors (P21 ， P27 ， P57) were up-regulat-ed in Rac1-V12-KG-1a cells at different level; moreover, the expressions of N-Cadherin and MPL were also signifi-cantly higher in Rac1-V12-KG-1a cells (P<0.05). Flow cytometry analysis showed that the percentage of G0 phase MPL + leukemia cells was significantly higher than that of MPL - leukemia cells ([40.3±3.5])% vs [19.05±7.65]%, P<0.05). Conclusion: Activation of Rac1 GTPase could increase the ratio of leukemia cells at G0 phase, and promote leukemia cells quiescence by up-regulating MPL.
Objective: To determine the role of Rac1 GTPase activation in the regulation of leukemia cell quies-cence and investigate the possible mechanism. Methods: Constitutively active Rac1 lenti-virus vector was construct-ed to transfect KG-1a leukemia cells (Rac1-V12-KG-1a). The G0 phase cell ratio in sorted Rac1-V12-KG-1a and KG-1a cells transfected with empty vector (pCDH-KG-1a) was compared. Furthermore, after 4 days treatment with NSC23766, the Rac1-specific inhibitor, the G0 phase cell ratio in KG-1a cells was also detected. The expression lev-els of cell quiescence and cell cycle associated moleculars were then determined by RT-PCR. The G0 phase cell ra-tio of MPL - and MPL + leukemia cells in AML1-ETO9a leukemia mouse was detected by flow cytometry. Results:The results showed that the G0 phase cell ratio in Rac1-V12-KG-1a cells was significantly higher than that in pCDH-KG-1a cells ([15.30±0.60]% vs [11.50 ± 0.17]%, P<0.05). After the treatment of Rac1-specific inhibitor, the G0 phase cell ratio of the KG-1a cells was decreased significantly (P<0.05), and the effect was concentration depen-dent. RT-PCR showed that mRNA transcription levels of cell cycle related factors (P21 ， P27 ， P57) were up-regulat-ed in Rac1-V12-KG-1a cells at different level; moreover, the expressions of N-Cadherin and MPL were also signifi-cantly higher in Rac1-V12-KG-1a cells (P<0.05). Flow cytometry analysis showed that the percentage of G0 phase MPL + leukemia cells was significantly higher than that of MPL - leukemia cells ([40.3±3.5])% vs [19.05±7.65]%, P<0.05). Conclusion: Activation of Rac1 GTPase could increase the ratio of leukemia cells at G0 phase, and promote leukemia cells quiescence by up-regulating MPL.
2017, 24(8):833-837.
DOI: 10.3872/j.issn.1007-385X.2017.08.003
Abstract:
Objective: To investigate the effect of siRNA targeting decoy receptor 3 gene on the radiosensitivity of pancreatic cancer cells and its related mechanism. Methods: Plasmid stably expressing DcR3 siRNA sequence was constructed and transfected into pancreatic cancer AsPC-1 cell line by liposome; control group, siRNA(-) negative control group and DcR3 siRNA group were set up. Then DcR3 expression in AsPC-1 cells was detected by Western blotting. Effect of DcR3 siRNA transfection on radiation sensitivity of AsPC-1 cells was detected by plate clone for-mation assay. Cell apoptosis was analyzed by Flow cytometry; the expressions of Caspase-8, Caspase-3 and PARP-1 were detected by Western blotting and RT-PCR after transfecting with DcR3 siRNA. Results: The expression of DcR3 protein in DcR3 siRNA group was significantly lower than that in control or siRNA(-) group (P<0.01). The colony formation rate of DcR3 siRNA group was significantly lower than that in control group and siRNA(-) group (P<0.01), and the survival fraction(SF) value of DcR3 siRNA group was decreased and the ratio of α/β was in-creased (P<0.01). The cell apoptosis rate of DcR3 siRNA group was significantly higher than that of control group or siRNA(-) group (P<0.01). DcR3 siRNA could significantly up-regulate the expression of Caspase-8 and Caspase-3 and down-egulatetheexpressionofPARP-.Conclusion:siRNAsilencingDcR3genecanincreasetheradiosensitiv-ityofpancreaticcancercellsbyactivatingthe apoptosis factors Caspase-8 and Caspase-3, promoting cell apoptosis.
Objective: To investigate the effect of siRNA targeting decoy receptor 3 gene on the radiosensitivity of pancreatic cancer cells and its related mechanism. Methods: Plasmid stably expressing DcR3 siRNA sequence was constructed and transfected into pancreatic cancer AsPC-1 cell line by liposome; control group, siRNA(-) negative control group and DcR3 siRNA group were set up. Then DcR3 expression in AsPC-1 cells was detected by Western blotting. Effect of DcR3 siRNA transfection on radiation sensitivity of AsPC-1 cells was detected by plate clone for-mation assay. Cell apoptosis was analyzed by Flow cytometry; the expressions of Caspase-8, Caspase-3 and PARP-1 were detected by Western blotting and RT-PCR after transfecting with DcR3 siRNA. Results: The expression of DcR3 protein in DcR3 siRNA group was significantly lower than that in control or siRNA(-) group (P<0.01). The colony formation rate of DcR3 siRNA group was significantly lower than that in control group and siRNA(-) group (P<0.01), and the survival fraction(SF) value of DcR3 siRNA group was decreased and the ratio of α/β was in-creased (P<0.01). The cell apoptosis rate of DcR3 siRNA group was significantly higher than that of control group or siRNA(-) group (P<0.01). DcR3 siRNA could significantly up-regulate the expression of Caspase-8 and Caspase-3 and down-egulatetheexpressionofPARP-.Conclusion:siRNAsilencingDcR3genecanincreasetheradiosensitiv-ityofpancreaticcancercellsbyactivatingthe apoptosis factors Caspase-8 and Caspase-3, promoting cell apoptosis.
2017, 24(8):838-844.
DOI: 10.3872/j.issn.1007-385X.2017.08.004
Abstract:
Objective: To investigate the expression of MicroRNA-150 (miR-150) in NK/T cell lymphoma tissues and its effect on radio-sensitivity of NK-92 cells. Methods: Thirty-six patients with NK/T cell lynphoma that treat-ed in Zhujiang Hospital Affiliated to Southern Medical University were included as study subjects, and their tissue samples were collected. All the patients received similar radiotherapy, and the short-term efficacy was evaluated by the standard of International Workgroup (IWG) of Lymphoma. The patients were further divided into CR (complete remission) group and Non-CR (non-complete remission) group according the treatment efficacy. The miR-150 ex-pression in lymphoma tissues and NK/T cell lymphoma cell lines were detected by qRT-PCR. The NK-92 cells were then transfected with miR-150 mimics. The effect of miR-150 mimics on NK-92 cell radiosensitivity was analyzed by MTT and colony formation assay; effect of miR-150 mimics on radiation induced apoptosis of NK-92 cells were analyzed by Flow Cytometry; and the effect of miR-150 mimics on the expression of apoptosis-related proteins (Cas-pase 3 and PARP) in NK-92 cells was determined by Western blotting. Results: According to IWG criteria, 12 pa-tients had CR while the other 24 patients had Non-CR. Compared with CR group, the microRNA-150 level in Non-CR group was significantly decreased(P<0.05). Compared with the normal sCD3 - CD56 + NK cells, miR-150 was sig-nificantly lower in NK/T cell lymphoma tissues (9.10 ±0.19 vs 4.01± 0.22 P<0.01 ) and five NK/T cell lymphoma cell lines (P<0.05); over-expression of miR-150 significantly decreased the proliferation and colony formation of NK-92 cells (all P<0.01), and increased the sensitivity enhancement ratio (SER) after radiation (the SER was 5.375 after 10 Gy exposure; in addition, over-expressions of miR-150 significantly promoted the radiation-induced apopto-sis of NK-92 cells [(37.3±1.24)% vs (28.3±2.34)%，P<0.05], and promoted the protein expression of caspase 3 and PARP in NK-92 cells. Conclusion: miR-150 expression significantly decreased in both NK/T cell lymphoms tissues and cell lines. The patients of low miR-150 expression had low CR after radiotherapy. miR-150 mimics transfection promoted radiation-induced apoptosis of NK-92 cells. miR-150 has an enhancement effect on radio-sensitivity of NK/T cell lynphoma.
Objective: To investigate the expression of MicroRNA-150 (miR-150) in NK/T cell lymphoma tissues and its effect on radio-sensitivity of NK-92 cells. Methods: Thirty-six patients with NK/T cell lynphoma that treat-ed in Zhujiang Hospital Affiliated to Southern Medical University were included as study subjects, and their tissue samples were collected. All the patients received similar radiotherapy, and the short-term efficacy was evaluated by the standard of International Workgroup (IWG) of Lymphoma. The patients were further divided into CR (complete remission) group and Non-CR (non-complete remission) group according the treatment efficacy. The miR-150 ex-pression in lymphoma tissues and NK/T cell lymphoma cell lines were detected by qRT-PCR. The NK-92 cells were then transfected with miR-150 mimics. The effect of miR-150 mimics on NK-92 cell radiosensitivity was analyzed by MTT and colony formation assay; effect of miR-150 mimics on radiation induced apoptosis of NK-92 cells were analyzed by Flow Cytometry; and the effect of miR-150 mimics on the expression of apoptosis-related proteins (Cas-pase 3 and PARP) in NK-92 cells was determined by Western blotting. Results: According to IWG criteria, 12 pa-tients had CR while the other 24 patients had Non-CR. Compared with CR group, the microRNA-150 level in Non-CR group was significantly decreased(P<0.05). Compared with the normal sCD3 - CD56 + NK cells, miR-150 was sig-nificantly lower in NK/T cell lymphoma tissues (9.10 ±0.19 vs 4.01± 0.22 P<0.01 ) and five NK/T cell lymphoma cell lines (P<0.05); over-expression of miR-150 significantly decreased the proliferation and colony formation of NK-92 cells (all P<0.01), and increased the sensitivity enhancement ratio (SER) after radiation (the SER was 5.375 after 10 Gy exposure; in addition, over-expressions of miR-150 significantly promoted the radiation-induced apopto-sis of NK-92 cells [(37.3±1.24)% vs (28.3±2.34)%，P<0.05], and promoted the protein expression of caspase 3 and PARP in NK-92 cells. Conclusion: miR-150 expression significantly decreased in both NK/T cell lymphoms tissues and cell lines. The patients of low miR-150 expression had low CR after radiotherapy. miR-150 mimics transfection promoted radiation-induced apoptosis of NK-92 cells. miR-150 has an enhancement effect on radio-sensitivity of NK/T cell lynphoma.
2017, 24(8):845-850.
DOI: 10.3872/j.issn.1007-385X.2017.08.005
Abstract:
Objective: To explore the expression of DNAJB8 （DnaJ heat shock protein family (Hsp40) member B8）in lung adenocarcinoma tissues and its effect on the invasion and migration of lung adenocarcinoma cells. Methods:102 surgical specimens resected from lung adenocarcinoma surgeries from 2006 to 2008 were collected at Sichuan Provincial People's Hospital, the expression of DNAJB8 in lung adenocarcinoma tissues was determined by immu-nohistochemistry (IHC), and its relationships with clinical pathological parameters and prognosis were analyzed.A549 cells with stable DNAJB8 knock down and H1299 cells with stable DNAJB8 overexpression were estab-lished; the effect of knockdown or overexpression of DNAJB8 on the proliferation of lung adenocarcinoma cells was evaluated by CCK-8 assay, the effect on the invasion ability of lung adenocarcinoma cells was determined us-ing Transwell assay, and the expression of invasion related proteins including MMP-2, MMP-9 and ERK were deter-mined by Western blotting; A xenograft model of lung adenocarcinoma was constructed on nude mice by injecting A549 cells with DNAJB8 knockdown via the tail vein to observe the effect of DNAJB8 on the migration of A549 cells in vivo. Results: The level of DNAJB8 expression in lung adenocarcinoma tissues was significantly higher than that in normal lung tissues, the high expression was positively correlated with lymph node metastasis and TNM staging, and predicted poor prognosis (P<0.01). The expression of DNAJB8 in A549 cells was higher than that in H1299 cells, and down-regulation of DNAJB8 expression inhibited the invasion of A549 cells ([41±3] vs [192±11]，P<0.01), while up-regulation of DNAJB8 promoted the invasion of H1299 cells ([235±14] vs [25±4]，P<0.01). The number of lung tumors in the mice of experimental group was significantly lower than that in the control group ([5±1] vs [17±3]，P<0.01). After DNAJB8 knockdown in A549 cells, the expressions of MMP-2, MMP-9 and p-ERK were decreased significantly (P<0.01); however, after the overexpression of DNAJB8 in H1299 cells, the expression of MMP-2, MMP-9 and p-ERK were significantly increased (P<0.01). Conclusion: DNAJB8 could promote the in-vasion and metastasis of lung adenocarcinoma cells, which is likely related with the MEK/Erk signaling pathway.
Objective: To explore the expression of DNAJB8 （DnaJ heat shock protein family (Hsp40) member B8）in lung adenocarcinoma tissues and its effect on the invasion and migration of lung adenocarcinoma cells. Methods:102 surgical specimens resected from lung adenocarcinoma surgeries from 2006 to 2008 were collected at Sichuan Provincial People's Hospital, the expression of DNAJB8 in lung adenocarcinoma tissues was determined by immu-nohistochemistry (IHC), and its relationships with clinical pathological parameters and prognosis were analyzed.A549 cells with stable DNAJB8 knock down and H1299 cells with stable DNAJB8 overexpression were estab-lished; the effect of knockdown or overexpression of DNAJB8 on the proliferation of lung adenocarcinoma cells was evaluated by CCK-8 assay, the effect on the invasion ability of lung adenocarcinoma cells was determined us-ing Transwell assay, and the expression of invasion related proteins including MMP-2, MMP-9 and ERK were deter-mined by Western blotting; A xenograft model of lung adenocarcinoma was constructed on nude mice by injecting A549 cells with DNAJB8 knockdown via the tail vein to observe the effect of DNAJB8 on the migration of A549 cells in vivo. Results: The level of DNAJB8 expression in lung adenocarcinoma tissues was significantly higher than that in normal lung tissues, the high expression was positively correlated with lymph node metastasis and TNM staging, and predicted poor prognosis (P<0.01). The expression of DNAJB8 in A549 cells was higher than that in H1299 cells, and down-regulation of DNAJB8 expression inhibited the invasion of A549 cells ([41±3] vs [192±11]，P<0.01), while up-regulation of DNAJB8 promoted the invasion of H1299 cells ([235±14] vs [25±4]，P<0.01). The number of lung tumors in the mice of experimental group was significantly lower than that in the control group ([5±1] vs [17±3]，P<0.01). After DNAJB8 knockdown in A549 cells, the expressions of MMP-2, MMP-9 and p-ERK were decreased significantly (P<0.01); however, after the overexpression of DNAJB8 in H1299 cells, the expression of MMP-2, MMP-9 and p-ERK were significantly increased (P<0.01). Conclusion: DNAJB8 could promote the in-vasion and metastasis of lung adenocarcinoma cells, which is likely related with the MEK/Erk signaling pathway.
QIAN Li
,
LIU Yang
,
LIU Lu
,
YE Feng
,
WANG Shaoqing
,
JIA Xiaoqin
,
FU Yi
,
GONG Weijuan
,
TIAN Fang
,
DING Jingjuan
,
XU Yuwei
2017, 24(8):851-855.
DOI: 10.3872/j.issn.1007-385X.2017.08.006
Abstract:
Objective: To study the cytolytic activity of myeloid-derived suppressor cell (MDSC) from BaF3-RAE1ε injected mice and its effect on the function of NK cell. Methods: Two derivatives of murine pro-B cell line BaF3 cells, expressing empty plasmid (termed BaF3-mock) or retinoic acid early transcript 1ε (RAE1ε, termed BaF3-RAE1ε) were respectively constructed in the previous study. CD11b + Gr-1 + MDSC magnetically purified from BaF3-mock or BaF3-RAE1ε bearing mice were co-cultured with NK cells. After 24 hours, the cells were harvested for detecting NKG2D and CD107a expression on NK cells by flow cytometry, and the supernatants were collected for detecting IFN-γ by ELISA. Moreover, MDSC sorted from BaF3-mock or BaF3-RAE1ε bearing mice were co-cultured with BaF3-mock or BaF3- RAE1ε target cells. After 5 h, the cytotoxicity of MDSC against BaF3-mock or BaF3-RAE1 target cells was evaluated by the lactate dehydrogenase release test. Results: There was no obvious dif-ference in secretion of IFN-γ by NK cells co-cultured with MDSC from BaF3-mock or BaF3-RAE1ε bearing mice (P＞0.05). No difference in NKG2D and CD107a expression was detected among NK cells co-cultured with MDSC from BaF3-mock or BaF3-RAE1ε bearing mice (P＞0.05). MDSC isolated from BaF3-RAE1ε bearing mice had higher direct cytolytic activity against BaF3-mock or BaF3-RAE1ε cells than MDSC isolated from BaF3-mock bear-ing mice (P<0.01). Conclusion: RAE1ε enhances the cytolytic activity of MDSC against BaF3-mock or BaF3-RAE1ε cells.
Objective: To study the cytolytic activity of myeloid-derived suppressor cell (MDSC) from BaF3-RAE1ε injected mice and its effect on the function of NK cell. Methods: Two derivatives of murine pro-B cell line BaF3 cells, expressing empty plasmid (termed BaF3-mock) or retinoic acid early transcript 1ε (RAE1ε, termed BaF3-RAE1ε) were respectively constructed in the previous study. CD11b + Gr-1 + MDSC magnetically purified from BaF3-mock or BaF3-RAE1ε bearing mice were co-cultured with NK cells. After 24 hours, the cells were harvested for detecting NKG2D and CD107a expression on NK cells by flow cytometry, and the supernatants were collected for detecting IFN-γ by ELISA. Moreover, MDSC sorted from BaF3-mock or BaF3-RAE1ε bearing mice were co-cultured with BaF3-mock or BaF3- RAE1ε target cells. After 5 h, the cytotoxicity of MDSC against BaF3-mock or BaF3-RAE1 target cells was evaluated by the lactate dehydrogenase release test. Results: There was no obvious dif-ference in secretion of IFN-γ by NK cells co-cultured with MDSC from BaF3-mock or BaF3-RAE1ε bearing mice (P＞0.05). No difference in NKG2D and CD107a expression was detected among NK cells co-cultured with MDSC from BaF3-mock or BaF3-RAE1ε bearing mice (P＞0.05). MDSC isolated from BaF3-RAE1ε bearing mice had higher direct cytolytic activity against BaF3-mock or BaF3-RAE1ε cells than MDSC isolated from BaF3-mock bear-ing mice (P<0.01). Conclusion: RAE1ε enhances the cytolytic activity of MDSC against BaF3-mock or BaF3-RAE1ε cells.
2017, 24(8):856-863.
DOI: 10.3872/j.issn.1007-385X.2017.08.007
Abstract:
Objective: To investigate the differentiation- inducing effect of melanoma differentiation associated gene 7（MDA-7）/IL-24 on human Burkitt lymphoma cells, as well as its underlying mechanism. Methods: Human Burkitt lymphoma cell lines (Raji and Daudi) that stably over-expressing MDA-7/IL-24 were constructed. The effect of MDA-7/IL-24 transfection on cell viability of Raji and Daudi cells was assayed by MTS method; the effect on mi-gration and invasion of Raji and Daudi cells were analyzed by Transwell assay. The apoptosis and immunopheno-types of Raji and Daudi cells with MDA-7/IL-24 over-expression were analyzed by flow cytometry. Meanwhile, the expressions of differentiation related proteins (Myb, BLIMP1 and BCL-6) were analyzed by Western blotting. Raji cell xenograft model was established on nude mice to analyze the effect of MDA-7/IL-24 on the bioactivity of Raji cells in vivo. Results: The cell viability, migration and invasion ability of Raji and Daudi cell lines that transfected with MDA-7/IL-24 were obviously decreased (all P<0.01), however, the apoptosis cells were not increased (P>0.05). The expressions of CD45 and CD138 were elevated (P<0.01) while the expression of CD10 was decreased (P<0.01) in Raji and Daudi cells overexpressing MDA-7/IL-24. MDA-7/IL-24 over-expression in Raji and Daudi cells significantly increased the expression of BLIMP1 (P<0.01), but decreased the expression of Myb and BCL-6(P＜0.01). The tumor mass of nude mice was significantly decreased after the treatment of MDA-7/IL-24 ([1.23±0.21] vs [1.96±0.24]g, P<0.01). Conclusion: Transfection with MDA-7/IL-24 inhibited the bio-actively of Burkitt lymphoma cells, which might be accomplished by inducing differentiation.
Objective: To investigate the differentiation- inducing effect of melanoma differentiation associated gene 7（MDA-7）/IL-24 on human Burkitt lymphoma cells, as well as its underlying mechanism. Methods: Human Burkitt lymphoma cell lines (Raji and Daudi) that stably over-expressing MDA-7/IL-24 were constructed. The effect of MDA-7/IL-24 transfection on cell viability of Raji and Daudi cells was assayed by MTS method; the effect on mi-gration and invasion of Raji and Daudi cells were analyzed by Transwell assay. The apoptosis and immunopheno-types of Raji and Daudi cells with MDA-7/IL-24 over-expression were analyzed by flow cytometry. Meanwhile, the expressions of differentiation related proteins (Myb, BLIMP1 and BCL-6) were analyzed by Western blotting. Raji cell xenograft model was established on nude mice to analyze the effect of MDA-7/IL-24 on the bioactivity of Raji cells in vivo. Results: The cell viability, migration and invasion ability of Raji and Daudi cell lines that transfected with MDA-7/IL-24 were obviously decreased (all P<0.01), however, the apoptosis cells were not increased (P>0.05). The expressions of CD45 and CD138 were elevated (P<0.01) while the expression of CD10 was decreased (P<0.01) in Raji and Daudi cells overexpressing MDA-7/IL-24. MDA-7/IL-24 over-expression in Raji and Daudi cells significantly increased the expression of BLIMP1 (P<0.01), but decreased the expression of Myb and BCL-6(P＜0.01). The tumor mass of nude mice was significantly decreased after the treatment of MDA-7/IL-24 ([1.23±0.21] vs [1.96±0.24]g, P<0.01). Conclusion: Transfection with MDA-7/IL-24 inhibited the bio-actively of Burkitt lymphoma cells, which might be accomplished by inducing differentiation.
LI Qian
,
WEI Zhihui
,
XIAO Qianren
,
CHEN Jiajun
,
ZHOU Xin
,
WANG Tengyu
,
ZHANG Zhongzu
,
ZHANG Minghua
2017, 24(8):864-869.
DOI: 10.3872/j.issn.1007-385X.2017.08.008
Abstract:
Objective: To explore the effects of miR-186 on the cell proliferation, apoptosis and invasion of hu-man osteosarcoma cells, and identify its putative mechanisms. Methods: The expression of miR-186 in osteosarco-ma cell lines (HOS, U2-OS and Saos-2) and osteoblast NHOst cells was detected using RT-PCR assays. Artificially synthesized miR-186 mimic and relative control scramble mimic was transfected into osteosarcoma HOS and U2-OS cell lines, and the expression of miR-186 in OS cells was detected using the RT-PCR assays upon transfection.Then, the effects of miR-186 over-expression on cell proliferation, apoptosis and invasion of OS cells were explored using the CCK-8, FCSE and transwell invasion assays, respectively. The effects of miR-186 over-expression on mRNAand protein expression of PTTG1 (pituitary tumor transforming gene1) were explored using the Western blot-ting and RT-PCR assays. Results: miR-186 was low expressed in OS cell lines; Transfection with artificially synthe-sized miR-186 mimic significantly up-regulated the expression of miR-186 in HOS and U2-OS cells; the prolifera-tion rate of cells transfected with miR-186 mimic was much lower than those transfected with scramble mimic [HOS: (16.9±2.1)% vs (10.4±1.6)%; U2-OS: (22.6±2.9)% vs (14.1±2.2)%; (P<0.01); the apoptotic rates of HOS and U2-OS cells transfected with miR-186 mimic were higher than those transfected with scramble mimic [HOS: (16.9±2.1)% vs (10.4±1.6)%; U2-OS: (22.6±2.9)% vs (14.1±2.2)%; all P<0.05], and the number of cells passing through the chambers in miR-186 mimic transfection group was less than those of scramble transfection group (P<0.01).The expression levels of PTTG1 at protein and mRNA level were both suppressed in cells transfected with miR-186 mimic (P<0.01); however, scramble transfection group showed no statistical difference (P>0.05). Conclusion: Over-expression of miR-186 significantly inhibited cell proliferation and invasion, and promoted the apoptosis of OS cells, which might be related with PTTG1 suppression.
Objective: To explore the effects of miR-186 on the cell proliferation, apoptosis and invasion of hu-man osteosarcoma cells, and identify its putative mechanisms. Methods: The expression of miR-186 in osteosarco-ma cell lines (HOS, U2-OS and Saos-2) and osteoblast NHOst cells was detected using RT-PCR assays. Artificially synthesized miR-186 mimic and relative control scramble mimic was transfected into osteosarcoma HOS and U2-OS cell lines, and the expression of miR-186 in OS cells was detected using the RT-PCR assays upon transfection.Then, the effects of miR-186 over-expression on cell proliferation, apoptosis and invasion of OS cells were explored using the CCK-8, FCSE and transwell invasion assays, respectively. The effects of miR-186 over-expression on mRNAand protein expression of PTTG1 (pituitary tumor transforming gene1) were explored using the Western blot-ting and RT-PCR assays. Results: miR-186 was low expressed in OS cell lines; Transfection with artificially synthe-sized miR-186 mimic significantly up-regulated the expression of miR-186 in HOS and U2-OS cells; the prolifera-tion rate of cells transfected with miR-186 mimic was much lower than those transfected with scramble mimic [HOS: (16.9±2.1)% vs (10.4±1.6)%; U2-OS: (22.6±2.9)% vs (14.1±2.2)%; (P<0.01); the apoptotic rates of HOS and U2-OS cells transfected with miR-186 mimic were higher than those transfected with scramble mimic [HOS: (16.9±2.1)% vs (10.4±1.6)%; U2-OS: (22.6±2.9)% vs (14.1±2.2)%; all P<0.05], and the number of cells passing through the chambers in miR-186 mimic transfection group was less than those of scramble transfection group (P<0.01).The expression levels of PTTG1 at protein and mRNA level were both suppressed in cells transfected with miR-186 mimic (P<0.01); however, scramble transfection group showed no statistical difference (P>0.05). Conclusion: Over-expression of miR-186 significantly inhibited cell proliferation and invasion, and promoted the apoptosis of OS cells, which might be related with PTTG1 suppression.
TANG Bixia
,
SI Lu
,
CHI Zhihong
,
SHENG Xinan
,
CUI Chuanliang
,
YAN Xieqiao
,
LI Siming
,
MAO Lili
,
LIAN Bin
,
WANG Xuan
,
BAI Xue
,
ZHOU Li
,
GUO Jun
2017, 24(8):870-874.
DOI: 10.3872/j.issn.1007-385X.2017.08.009
Abstract:
Objective: To investigate the application value of temozolomide (TMZ) combined with sunitinib (SUN)in the treatment of metastatic mucosal melanoma. Methods: This research retrospectively analyzed the data of pa-tients with metastatic mucosal melanoma that treated with TMZ combined with SUN in Peking University Cancer Hospital from August, 2008 to December, 2016. Patients showed no BRAF/NRAS mutation. The combination regi-men of SUN (37.5 mg, d1-28) and TMZ (200 mg/m 2 , d1-5) was continued in a 28-days cycle until disease progres-sion or toxicity intolerance. The primary observation indices were objective response rate (ORR), progression-free survival (PFS), overall survival (OS) and toxic side effect rate. Results: Among the included 27 patients, primary in-testinal lesion occurred in 4 patients, genitourinary lesion occurred in 9 patient, nasal lesions in 5 patient, oral le-sions in 7 patients and esophagal lesion in 2 patients; 19 patients had been previously treated with anti-tumor treat-ment. Median treatment cycle was 3.0 of TMZ combined with SUN treatment. ORR was 19.2%, disease control rate was 81.5%, median PFS and OS were (3.0±0.7) months and (7.1±0.9) months, respectively. KIT mutation was de-tected in 4 patients, and the use of KIT inhibitor might be beneficial to those patients. The combination therapy was well tolerated, and only 2 patients required a dose reduction of SUN to 25 mg due to thrombocytopenia (grade Ⅳ).Grade Ⅲ-Ⅳ toxicities mainly included thrombocytopenia (19.2%), leucopenia (19.2%), and hepatic injury (3.9%).No treatment related death occurred. Conclusion: For metastatic mucosal melanoma, TMZ+SUN might be an effec-tive and safe approach.
Objective: To investigate the application value of temozolomide (TMZ) combined with sunitinib (SUN)in the treatment of metastatic mucosal melanoma. Methods: This research retrospectively analyzed the data of pa-tients with metastatic mucosal melanoma that treated with TMZ combined with SUN in Peking University Cancer Hospital from August, 2008 to December, 2016. Patients showed no BRAF/NRAS mutation. The combination regi-men of SUN (37.5 mg, d1-28) and TMZ (200 mg/m 2 , d1-5) was continued in a 28-days cycle until disease progres-sion or toxicity intolerance. The primary observation indices were objective response rate (ORR), progression-free survival (PFS), overall survival (OS) and toxic side effect rate. Results: Among the included 27 patients, primary in-testinal lesion occurred in 4 patients, genitourinary lesion occurred in 9 patient, nasal lesions in 5 patient, oral le-sions in 7 patients and esophagal lesion in 2 patients; 19 patients had been previously treated with anti-tumor treat-ment. Median treatment cycle was 3.0 of TMZ combined with SUN treatment. ORR was 19.2%, disease control rate was 81.5%, median PFS and OS were (3.0±0.7) months and (7.1±0.9) months, respectively. KIT mutation was de-tected in 4 patients, and the use of KIT inhibitor might be beneficial to those patients. The combination therapy was well tolerated, and only 2 patients required a dose reduction of SUN to 25 mg due to thrombocytopenia (grade Ⅳ).Grade Ⅲ-Ⅳ toxicities mainly included thrombocytopenia (19.2%), leucopenia (19.2%), and hepatic injury (3.9%).No treatment related death occurred. Conclusion: For metastatic mucosal melanoma, TMZ+SUN might be an effec-tive and safe approach.
2017, 24(8):875-879.
DOI: 10.3872/j.issn.1007-385X.2017.08.010
Abstract:
Objective: The aim of this study was to determine the expression of zinc finger protein of the cerebellum 1 (ZIC1) in endometrial cancer tissues, and to investigate its correlation to clinical parameters as well as it prognostic value. Methods: We selected 43 endometrial cancer patients from Kunshan First People’s Hospital Affiliated to Ji-angsu University and Shanghai No.6 People’s Hospital during January 2008 to November 2011, and collected tumor tissues and corresponding para-carcinoma tissues (2 cm or more away from the primary lesion). Immunohistochemis-try, Western blotting and RT-PCR were used to determine the expressions of ZIC1 in 43 endometrial cancer samples as well as the normal adjacent tissues; the association between ZICI expression and clinicopathological parameters were analyzed, and its prognostic value was investigated through 5-year survival analysis. Results:Asignificantly in-creased expression of ZIC1 was observed in endometrial cancer tissues compared to that in para-carcinoma tissues,for both mRNAand protein levels through RT-PCR and Western blotting (P<0.05). ZIC1 was highly expressed in en-dometrial cancer samples with a positive rate of 72.1% (31/43), while the positive rate in para-carcinoma tissues were 39.5% (17/43). Moreover, ZIC1 mRNAwas significantly correlated with lymph node metastasis and FIGO stag-ing (P<0.05); the 5-year survival of ZIC1 - patients was significantly higher than that of ZIC1+patients (66.7% vs 38.7%，P<0.05). Univariant analysis revealed that the hazard ratio (HR) of ZIC1 (high expression vs low expression)was 2.66, 95%CI: 1.07-5.89，P=0.047; and after the adjustment of multivariate analysis, the result showed HR=2.25，95%CI: 1.36-3.71，P=0.002, indicating high level ZIC1 was closely related to the poor prognosis after endometrial surgery. Conclusions: ZIC1 plays an important role in the occurrence and development of endometrial adenocarcino-ma and may be served as a promising target for the therapy and prognosis of endometrial adenocarcinoma.
Objective: The aim of this study was to determine the expression of zinc finger protein of the cerebellum 1 (ZIC1) in endometrial cancer tissues, and to investigate its correlation to clinical parameters as well as it prognostic value. Methods: We selected 43 endometrial cancer patients from Kunshan First People’s Hospital Affiliated to Ji-angsu University and Shanghai No.6 People’s Hospital during January 2008 to November 2011, and collected tumor tissues and corresponding para-carcinoma tissues (2 cm or more away from the primary lesion). Immunohistochemis-try, Western blotting and RT-PCR were used to determine the expressions of ZIC1 in 43 endometrial cancer samples as well as the normal adjacent tissues; the association between ZICI expression and clinicopathological parameters were analyzed, and its prognostic value was investigated through 5-year survival analysis. Results:Asignificantly in-creased expression of ZIC1 was observed in endometrial cancer tissues compared to that in para-carcinoma tissues,for both mRNAand protein levels through RT-PCR and Western blotting (P<0.05). ZIC1 was highly expressed in en-dometrial cancer samples with a positive rate of 72.1% (31/43), while the positive rate in para-carcinoma tissues were 39.5% (17/43). Moreover, ZIC1 mRNAwas significantly correlated with lymph node metastasis and FIGO stag-ing (P<0.05); the 5-year survival of ZIC1 - patients was significantly higher than that of ZIC1+patients (66.7% vs 38.7%，P<0.05). Univariant analysis revealed that the hazard ratio (HR) of ZIC1 (high expression vs low expression)was 2.66, 95%CI: 1.07-5.89，P=0.047; and after the adjustment of multivariate analysis, the result showed HR=2.25，95%CI: 1.36-3.71，P=0.002, indicating high level ZIC1 was closely related to the poor prognosis after endometrial surgery. Conclusions: ZIC1 plays an important role in the occurrence and development of endometrial adenocarcino-ma and may be served as a promising target for the therapy and prognosis of endometrial adenocarcinoma.
11 MicroRNA-99a promotes proliferation and migration of colon cancer cell and its anti-tumor mechanism
2017, 24(8):880-883.
DOI: 10.3872/j.issn.1007-385X.2017.08.011
Abstract:
Objective: To investigate the expression of microRNA-99a in the tumor tissues of colon cancer patients and its effect on cancer cell proliferation and migration. Methods: 49 pairs of cancer tissue and adjacent tissue (5 cm away from cancer tissue) from colon cancer patients that treated in Gastrointestinal Center of Affiliated Chang-zhou Second Hospital of Nanjing Medical University, and colon cancer cell lines (HT-29，HCT-116，SW480，Caco-2) as well as normal epithelial HcoePic cell line were selected for our research. Quantitative real-time PCR was used to detect the levels of microRNA-99a in tumor tissues, adjacent tissues and tumor cells; After transfection of mc-iroRNA-99a inhibitor, we used CCK-8 to test the cell proliferation, transwell assay to observe the cell migration,and Western lotting to examine the levels of FGFR3 in HT-29 cells. Results: The expression of microRNA-99a in the cancer tissues was significantly higher than that in normal para-cancerous tissues (6.27±0.48 vs 1.34±0.54, P<0.05), and its expression in tumor cells was significantly higher than that in normal colon epithelial cells（5.48±0.34, 7.67±0.24, 5.78±0.22, 6.28±0.44 vs 1.45±0.37, P<0.05). After microRNA-99a inhibitor transfection, cell pro-liferation and migration of HT-29 cells were significantly decreased (P<0.05); , in the meanwhile, the mRNA and protein levels of FGFR3 were significantly decreased in HT-29 cells (P<0.05). Conclusion: microRNA-99a was highly expressed in the tumor tissue of colon cancer patients and colon cancer cells, and low expression of microR-NA-99a may weaken the proliferation and migration ability of cancer cells, which might be accomplished throughFGFR3 signaling pathway.
Objective: To investigate the expression of microRNA-99a in the tumor tissues of colon cancer patients and its effect on cancer cell proliferation and migration. Methods: 49 pairs of cancer tissue and adjacent tissue (5 cm away from cancer tissue) from colon cancer patients that treated in Gastrointestinal Center of Affiliated Chang-zhou Second Hospital of Nanjing Medical University, and colon cancer cell lines (HT-29，HCT-116，SW480，Caco-2) as well as normal epithelial HcoePic cell line were selected for our research. Quantitative real-time PCR was used to detect the levels of microRNA-99a in tumor tissues, adjacent tissues and tumor cells; After transfection of mc-iroRNA-99a inhibitor, we used CCK-8 to test the cell proliferation, transwell assay to observe the cell migration,and Western lotting to examine the levels of FGFR3 in HT-29 cells. Results: The expression of microRNA-99a in the cancer tissues was significantly higher than that in normal para-cancerous tissues (6.27±0.48 vs 1.34±0.54, P<0.05), and its expression in tumor cells was significantly higher than that in normal colon epithelial cells（5.48±0.34, 7.67±0.24, 5.78±0.22, 6.28±0.44 vs 1.45±0.37, P<0.05). After microRNA-99a inhibitor transfection, cell pro-liferation and migration of HT-29 cells were significantly decreased (P<0.05); , in the meanwhile, the mRNA and protein levels of FGFR3 were significantly decreased in HT-29 cells (P<0.05). Conclusion: microRNA-99a was highly expressed in the tumor tissue of colon cancer patients and colon cancer cells, and low expression of microR-NA-99a may weaken the proliferation and migration ability of cancer cells, which might be accomplished throughFGFR3 signaling pathway.
2017, 24(8):884-888.
DOI: 10.3872/j.issn.1007-385X.2017.08.012
Abstract:
Objective: To investigate the expression and clinical significance of lncRNA NCRNA00173 in the tis-sues of osteosarcoma patients. Methods: The expression of lncRNA NCRNA00173 mRNA was detected in 54 cases of osteosarcoma tissues and adjacent tissues (collected from the patients underwent surgery between October, 2012 and December, 2016 at the Department of Orthopedic, Sichuan Provincial People’s Hospital) by real-time fluores-cence quantification PCR, and its clinical significance was analyzed. Results: The expression of lncRNA NCRNA00173 in osteosarcoma tissues was obviously decreased compared with that in paracarcinoma tissues (1.793±0.158 vs 5.368±0.285，t=10.96，P<0.01). LncRNA NCRNA00173 expression was not significantly correlat-ed with patients’gender or age (both P>0.05), but remarkably correlated with disease stage, distant metastasis, tu-mor differentiation and the survival (all P<0.05); Furthermore, patients with high lncRNA NCRNA00173 expres-sion had significant longer OS and median PFS. Cox multivariate regression analysis suggested that lncRNA NCRNA00173 expression, distant metastasis and clinical stage were the independent prognostic factors for osteosar-coma (P<0.05). Conclusion: lncRNA NCRNA00173 is involved in the occurrence and development of osteosarco-ma, and can be used as a molecular marker for the diagnosis and prognosis of osteosarcoma.
Objective: To investigate the expression and clinical significance of lncRNA NCRNA00173 in the tis-sues of osteosarcoma patients. Methods: The expression of lncRNA NCRNA00173 mRNA was detected in 54 cases of osteosarcoma tissues and adjacent tissues (collected from the patients underwent surgery between October, 2012 and December, 2016 at the Department of Orthopedic, Sichuan Provincial People’s Hospital) by real-time fluores-cence quantification PCR, and its clinical significance was analyzed. Results: The expression of lncRNA NCRNA00173 in osteosarcoma tissues was obviously decreased compared with that in paracarcinoma tissues (1.793±0.158 vs 5.368±0.285，t=10.96，P<0.01). LncRNA NCRNA00173 expression was not significantly correlat-ed with patients’gender or age (both P>0.05), but remarkably correlated with disease stage, distant metastasis, tu-mor differentiation and the survival (all P<0.05); Furthermore, patients with high lncRNA NCRNA00173 expres-sion had significant longer OS and median PFS. Cox multivariate regression analysis suggested that lncRNA NCRNA00173 expression, distant metastasis and clinical stage were the independent prognostic factors for osteosar-coma (P<0.05). Conclusion: lncRNA NCRNA00173 is involved in the occurrence and development of osteosarco-ma, and can be used as a molecular marker for the diagnosis and prognosis of osteosarcoma.
2017, 24(8):889-894.
DOI: 10.3872/j.issn.1007-385X.2017.08.013
Abstract:
Objective: To investigate the expression and clinical significance of lncRNA CRNDE (colorectal neo-plasia differentially expressed) in NSCLC(non-small cell lung cancer) tissues. Methods: 137 cases of NSCLC tis-sues and corresponding para-cancerous tissues from patients with NSCLC who underwent radical or palliative resec-tion in General Hospital of Chengdu Military Region from January 1，2011 to December 31, 2015 were collected for this study; Meanwhile, 29 cases of normal lung tissues from patients suffered from traumatic injury were used as controls. The expression of lncRNA CRNDE in 137 cases of NSCLC tissues and adjacent tissues were detected by QRT-PCR method, and the relationship between its expression and clinical pathological characteristics and progno-sis of NSCLC were analyzed. Results: Compared with the para-cancerous tissues (1.098±0.082), the average expres-sion level of lncRNA CRNDE in cancer tissues (5.283±0.245) was significantly higher with statistical significance (t=14.59, P<0.001). lncRNA CRNDE expression was significantly correlated with disease stage, distant metastasis,pathological type and survival status (all P<0.05), but not associated with age, gender, smoking, tumor size, lymph node metastasis and tumor difference (all P>0.05). The high lncRNA CRNDE expression was related to the patho-logical type of NSCLC (P< 0.05), and the expression of lncRNA CRNDE in adenocarcinoma group was significant-ly higher than that in squamous cell carcinoma and other groups. Moreover, Kaplan-Meier analysis demonstrated that the progression-free survival time in patients with high lncRNA CRNDE expression (20±1.72 months) was shortened compared with the patients with low expression (34.07±1.97 months), the difference was statistically sig-nificant (χ 2 =15.940, P<0.001); the overall survival time of patients with low lncRNA CRNDE expression (47.50±2.31 months) was significantly prolonged compared with those patients with high expression (32.15±2.19 months),the difference was statistically significant (χ 2 =12.40, P=0.004). Cox multivariate survival analysis also indicated that lncRNA CRNDE expression, distant metastasis, clinical stage were the independent prognostic markers for NSCLC (P<0.05). Conclusion: lncRNA CRNDE is involved in the occurrence and development of NSCLC, and can be used as a biomarker for the diagnosis and prognosis of non-small cell lung cancer.
Objective: To investigate the expression and clinical significance of lncRNA CRNDE (colorectal neo-plasia differentially expressed) in NSCLC(non-small cell lung cancer) tissues. Methods: 137 cases of NSCLC tis-sues and corresponding para-cancerous tissues from patients with NSCLC who underwent radical or palliative resec-tion in General Hospital of Chengdu Military Region from January 1，2011 to December 31, 2015 were collected for this study; Meanwhile, 29 cases of normal lung tissues from patients suffered from traumatic injury were used as controls. The expression of lncRNA CRNDE in 137 cases of NSCLC tissues and adjacent tissues were detected by QRT-PCR method, and the relationship between its expression and clinical pathological characteristics and progno-sis of NSCLC were analyzed. Results: Compared with the para-cancerous tissues (1.098±0.082), the average expres-sion level of lncRNA CRNDE in cancer tissues (5.283±0.245) was significantly higher with statistical significance (t=14.59, P<0.001). lncRNA CRNDE expression was significantly correlated with disease stage, distant metastasis,pathological type and survival status (all P<0.05), but not associated with age, gender, smoking, tumor size, lymph node metastasis and tumor difference (all P>0.05). The high lncRNA CRNDE expression was related to the patho-logical type of NSCLC (P< 0.05), and the expression of lncRNA CRNDE in adenocarcinoma group was significant-ly higher than that in squamous cell carcinoma and other groups. Moreover, Kaplan-Meier analysis demonstrated that the progression-free survival time in patients with high lncRNA CRNDE expression (20±1.72 months) was shortened compared with the patients with low expression (34.07±1.97 months), the difference was statistically sig-nificant (χ 2 =15.940, P<0.001); the overall survival time of patients with low lncRNA CRNDE expression (47.50±2.31 months) was significantly prolonged compared with those patients with high expression (32.15±2.19 months),the difference was statistically significant (χ 2 =12.40, P=0.004). Cox multivariate survival analysis also indicated that lncRNA CRNDE expression, distant metastasis, clinical stage were the independent prognostic markers for NSCLC (P<0.05). Conclusion: lncRNA CRNDE is involved in the occurrence and development of NSCLC, and can be used as a biomarker for the diagnosis and prognosis of non-small cell lung cancer.
REN Xianxian
,
LI Xia
,
XIAO Yongbiao
,
ZHU Junling
,
Mikairemu·Maimaiti
,
XU Jie
,
PAN Zemin
,
CAO Dongdong
,
LI Dongmei
2017, 24(8):895-899.
DOI: 10.3872/j.issn.1007-385X.2017.08.014
Abstract:
Objective: To detect the expression of HuR (human antigen R) protein in normal gastric mucosa and gastric cancer tissues of Uygur population, and to analyze the relationship between HuR protein and clinicopatholog-ical factors of gastric cancer. Methods: Thirty cases of paraffin embedded gastric tissue samples and 23 cases of cor-responding normal gastric mucosa specimens from First People's Hospital of Kashgar region were collected for this study. The expression levels of HuR in gastric cancer tissues and normal gastric mucosa tissues were examined by tissue microarray and immunohistochemistry SP method; concentrations of AFP, CEA, CA199 and SCC in serum of the patients with gastric cancer were examined by electrochemical luminescence assay. The relationship between HuR expression and clinicopathological characteristics as well as expression of tumor markers in gastric cancer pa-tients were analyzed. Results: HuR was expressed both in the cytoplasm and nucleus of the gastric cancer cells. The positive expression of HuR in nucleus of gastric cancer cells was 83.33%, which was significantly higher than that in normal gastric mucosa cell (52.17%, P<0.05); However, the protein expression was not correlated with the clini-copathological stage of gastric cancer. HuR expression in cytoplasm of gastric cancer cells was 70%, which was sig-nificantly higher than that in normal gastric mucosa (34.78%, (P<0.05), and was correlated with lymph node metas-tasis and clinical stage (P<0.05); In addition, its expression was associated with tumor marker CA199 (P<0.05). Conclusion: In Uygur population, the expression of HuR is highly expressed in the nuclei and cytoplasm of gastric cancer cells, which is significantly higher than that in normal gastric mucosa cells. Moreover, HuR expression in cy-toplasm is associated with lynphonode metastasis, clinical staging and tumor marker CA199.
Objective: To detect the expression of HuR (human antigen R) protein in normal gastric mucosa and gastric cancer tissues of Uygur population, and to analyze the relationship between HuR protein and clinicopatholog-ical factors of gastric cancer. Methods: Thirty cases of paraffin embedded gastric tissue samples and 23 cases of cor-responding normal gastric mucosa specimens from First People's Hospital of Kashgar region were collected for this study. The expression levels of HuR in gastric cancer tissues and normal gastric mucosa tissues were examined by tissue microarray and immunohistochemistry SP method; concentrations of AFP, CEA, CA199 and SCC in serum of the patients with gastric cancer were examined by electrochemical luminescence assay. The relationship between HuR expression and clinicopathological characteristics as well as expression of tumor markers in gastric cancer pa-tients were analyzed. Results: HuR was expressed both in the cytoplasm and nucleus of the gastric cancer cells. The positive expression of HuR in nucleus of gastric cancer cells was 83.33%, which was significantly higher than that in normal gastric mucosa cell (52.17%, P<0.05); However, the protein expression was not correlated with the clini-copathological stage of gastric cancer. HuR expression in cytoplasm of gastric cancer cells was 70%, which was sig-nificantly higher than that in normal gastric mucosa (34.78%, (P<0.05), and was correlated with lymph node metas-tasis and clinical stage (P<0.05); In addition, its expression was associated with tumor marker CA199 (P<0.05). Conclusion: In Uygur population, the expression of HuR is highly expressed in the nuclei and cytoplasm of gastric cancer cells, which is significantly higher than that in normal gastric mucosa cells. Moreover, HuR expression in cy-toplasm is associated with lynphonode metastasis, clinical staging and tumor marker CA199.
2017, 24(8):900-903.
DOI: 10.3872/j.issn.1007-385X.2017.08.015
Abstract:
Objective: To observe the mRNA and protein expressions of RNA-binding motif protein 38 (RBM38 or RNPC1) and tumor suppressor gene p53 in lung adenocarcinoma tissues, and to explore its significance in the occur-rence and development of lung adenocarcinoma. Methods: Tumor tissue samples from 50 lung adenocarcinoma pa-tients that treated in Affiliated Tumor Hospital of Xinjiang Medical University were selected as the experiment group, and the corresponding adjacent tissue samples were taken as the control group. The relative mRNA expres-sion of RBM38 and p53 in two groups were detected by RT-PCR method, and the relative protein expression of RBM38 and p53 were detected by Western blotting. Results: The mRNA and protein expressions of of RBM38 in the experimental group (0.357±0.170, 0.294±0.149) were higher than those of the control group (0.271±0.128,0.206±0.099), and the mRNA and protein expressions of p53 (0.457±0.208, 0.671±0.200) were higher than those of control group (0.308±0.167, 0.332±0.071); The difference was statistically significant (all P < 0.01). RBM38 expres-sion was related to TNM stage and depth of invasion in patients with lung adenocarcinoma (P < 0.05). The expres-sion of p53 was related to the TNM staging of the patients (P<0.05). The expression of RBM38 and p53 protein in the experience group were correlated (r=- 0.626, P<0.01). Conclusion: The mRNA and protein expressions of RBM38 and p53 in lung adenocarcinoma tissues were higher than that in adjacent tissues, and they were closely re-lated to the pathological parameters of the patients, such as TNM staging. With the increase of RBM38 protein ex-pression and decrease of p53 protein, RBM38 may promote the occurrence and development of lung cancer by in-hibiting the translation of p53. RBM38 may be the target of molecular targeted therapy for lung adenocarcinoma.
Objective: To observe the mRNA and protein expressions of RNA-binding motif protein 38 (RBM38 or RNPC1) and tumor suppressor gene p53 in lung adenocarcinoma tissues, and to explore its significance in the occur-rence and development of lung adenocarcinoma. Methods: Tumor tissue samples from 50 lung adenocarcinoma pa-tients that treated in Affiliated Tumor Hospital of Xinjiang Medical University were selected as the experiment group, and the corresponding adjacent tissue samples were taken as the control group. The relative mRNA expres-sion of RBM38 and p53 in two groups were detected by RT-PCR method, and the relative protein expression of RBM38 and p53 were detected by Western blotting. Results: The mRNA and protein expressions of of RBM38 in the experimental group (0.357±0.170, 0.294±0.149) were higher than those of the control group (0.271±0.128,0.206±0.099), and the mRNA and protein expressions of p53 (0.457±0.208, 0.671±0.200) were higher than those of control group (0.308±0.167, 0.332±0.071); The difference was statistically significant (all P < 0.01). RBM38 expres-sion was related to TNM stage and depth of invasion in patients with lung adenocarcinoma (P < 0.05). The expres-sion of p53 was related to the TNM staging of the patients (P<0.05). The expression of RBM38 and p53 protein in the experience group were correlated (r=- 0.626, P<0.01). Conclusion: The mRNA and protein expressions of RBM38 and p53 in lung adenocarcinoma tissues were higher than that in adjacent tissues, and they were closely re-lated to the pathological parameters of the patients, such as TNM staging. With the increase of RBM38 protein ex-pression and decrease of p53 protein, RBM38 may promote the occurrence and development of lung cancer by in-hibiting the translation of p53. RBM38 may be the target of molecular targeted therapy for lung adenocarcinoma.
2017, 24(8):904-911.
DOI: 10.3872/j.issn.1007-385X.2017.08.016
Abstract:
近年来，程序死亡分子（programmed death-1,PD1）/PD1配体（PD1 ligand，PD-L1）抑制剂在黑色素瘤的治疗中取得了突破性进展，并迅速应用到其他类型肿瘤，其中包括肺癌、乳腺癌、肝癌、胰腺癌、消化道肿瘤、妇科肿瘤、泌尿系统肿瘤以及骨髓瘤和淋巴瘤等多种恶性肿瘤，许多临床试验证明了抗PD1/PD-L1治疗可显著改善癌症患者生存期，并且治疗相关不良反应耐受性尚可。目前关于其抗肿瘤活性及安全性的研究仍在继续，并进一步探索其诊断、疗效评估的理想生物标记物，以及用于长期监测的方法，期待这些问题的解决，使抗PD1/PD-L1治疗更加系统、完善，为更多的癌症患者带来生存获益。
近年来，程序死亡分子（programmed death-1,PD1）/PD1配体（PD1 ligand，PD-L1）抑制剂在黑色素瘤的治疗中取得了突破性进展，并迅速应用到其他类型肿瘤，其中包括肺癌、乳腺癌、肝癌、胰腺癌、消化道肿瘤、妇科肿瘤、泌尿系统肿瘤以及骨髓瘤和淋巴瘤等多种恶性肿瘤，许多临床试验证明了抗PD1/PD-L1治疗可显著改善癌症患者生存期，并且治疗相关不良反应耐受性尚可。目前关于其抗肿瘤活性及安全性的研究仍在继续，并进一步探索其诊断、疗效评估的理想生物标记物，以及用于长期监测的方法，期待这些问题的解决，使抗PD1/PD-L1治疗更加系统、完善，为更多的癌症患者带来生存获益。
2017, 24(8):912-917.
DOI: 10.3872/j.issn.1007-385X.2017.08.017
Abstract:
肿瘤干细胞(cancer stem cell, CSC)是一类能持续自我更新并保持分化潜能的细胞，是影响恶性肿瘤形成、增殖、转移、复发的重要因素，并在肿瘤发生发展中起主导作用。研究发现，CSC的生理学功能可受到基因、微环境的影响，除此之外，自噬对维持CSC的存活、分化潜能及维护肿瘤微环境稳定也发挥了重要作用，并且CSC的自噬过程对肿瘤的发生及转移也有重要影响。
肿瘤干细胞(cancer stem cell, CSC)是一类能持续自我更新并保持分化潜能的细胞，是影响恶性肿瘤形成、增殖、转移、复发的重要因素，并在肿瘤发生发展中起主导作用。研究发现，CSC的生理学功能可受到基因、微环境的影响，除此之外，自噬对维持CSC的存活、分化潜能及维护肿瘤微环境稳定也发挥了重要作用，并且CSC的自噬过程对肿瘤的发生及转移也有重要影响。
2017, 24(8):918-922.
DOI: 10.3872/j.issn.1007-385X.2017.08.018
Abstract:
循环肿瘤DNA(circulating tumor DNA，ctDNA)是由实体肿瘤细胞释放到循环系统中的基因组小片段，来源于机体内所有肿瘤部位，其携带的基因组信息与肿瘤组织具有良好的一致性，能克服常规肿瘤组织活检所无法突破的肿瘤异质性问题。通过外周血ctDNA检测可以进行肿瘤相关基因的遗传学和表观遗传学研究，如基因突变、异常扩增、杂合性缺失等，还可以进行定量，追踪机体内特异性基因的状态变化。ctDNA检测是一种新兴技术，相对于传统的肿瘤组织活检具有简单、易行、高重复性等优点，更易被患者接受。目前主要的技术及平台包括PCR技术和二代测序法，两者各有所长，根据不同时期不同需求可以进行调整。ctDNA检测在结直肠癌的早期诊断、疗效评估、动态监测、耐药评估以及个体化精准治疗中具有深远意义及临床价值。
循环肿瘤DNA(circulating tumor DNA，ctDNA)是由实体肿瘤细胞释放到循环系统中的基因组小片段，来源于机体内所有肿瘤部位，其携带的基因组信息与肿瘤组织具有良好的一致性，能克服常规肿瘤组织活检所无法突破的肿瘤异质性问题。通过外周血ctDNA检测可以进行肿瘤相关基因的遗传学和表观遗传学研究，如基因突变、异常扩增、杂合性缺失等，还可以进行定量，追踪机体内特异性基因的状态变化。ctDNA检测是一种新兴技术，相对于传统的肿瘤组织活检具有简单、易行、高重复性等优点，更易被患者接受。目前主要的技术及平台包括PCR技术和二代测序法，两者各有所长，根据不同时期不同需求可以进行调整。ctDNA检测在结直肠癌的早期诊断、疗效评估、动态监测、耐药评估以及个体化精准治疗中具有深远意义及临床价值。
2017, 24(8):923-925.
DOI: 10.3872/j.issn.1007-385X.2017.08.019
Abstract:
联系方式
- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
- 国内定价： ￥20元/册
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.