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Volume 25,Issue 10,2018 Table of Contents
2018, 25(10):967-978.
DOI: 10.3872/j.issn.1007-385X.2018.10.001
Abstract:
[Abstract] Colorectal cancer (CRC) is the third most common malignancy and the fourth leading cause of cancer-related death all over the world. Traditional treatments, including chemotherapy, radiation therapy, surgery and targeted therapy, form the backbone of current treatment in various stages of CRC, but the efficacy in patients with recurrent or metastatic disease is extremely poor. Recently-developed immunotherapy is frequently used in various cancers with high malignancy, such as leukemia, melanoma and non-small-cell lung cancer, and achieves promising clinical outcomes. Immunotherapy has been also investigated in CRC, but the outcome is so disappointed in majority of patients, except the PD-1 inhibitor achieved excellent result in CRC with DNA mismatch repair system deficiency. In this review, the authors will mainly introduce the immunophenotype of different subtype of CRC and summarize current advances of clinical trials for CRC immunotherapy. The article will also discuss the reasons for the low efficacy of immunotherapeutic approaches in CRC and provide several potential directions for the future development of CRC immunotherapy.
[Abstract] Colorectal cancer (CRC) is the third most common malignancy and the fourth leading cause of cancer-related death all over the world. Traditional treatments, including chemotherapy, radiation therapy, surgery and targeted therapy, form the backbone of current treatment in various stages of CRC, but the efficacy in patients with recurrent or metastatic disease is extremely poor. Recently-developed immunotherapy is frequently used in various cancers with high malignancy, such as leukemia, melanoma and non-small-cell lung cancer, and achieves promising clinical outcomes. Immunotherapy has been also investigated in CRC, but the outcome is so disappointed in majority of patients, except the PD-1 inhibitor achieved excellent result in CRC with DNA mismatch repair system deficiency. In this review, the authors will mainly introduce the immunophenotype of different subtype of CRC and summarize current advances of clinical trials for CRC immunotherapy. The article will also discuss the reasons for the low efficacy of immunotherapeutic approaches in CRC and provide several potential directions for the future development of CRC immunotherapy.
2018, 25(10):979-986.
DOI: 10.3872/j.issn.1007-385X.2018.10.002
Abstract:
[Abstract] At present, more and more evidence shows that colon and rectal cancers are different diseases. There are many differences no matter in the epidemiology, anatomy and histology, molecular characteristics, transfer patterns, or clinical treatment methods, therapeutic effects and prognosis. In clinical treatment, it cann’t be considered as the same disease in general. Through the retrospective analysis of the three clinical studies of CALGB/SWOG 80405, CRYSTAL, and FIRE-3, it has been found that there were significant differences in the efficacy of cetuximab and bevacizumab in left and right colon cancer. Based on the above clinical trials, the National Cancer Institute for the United States (NCCN) for the first time includes the guidelines for the impact of primary sites on the treatment of colon cancer into guidelines in 2017. In the current era of advocating precision and individualized treatment, to clarify the pathogenesis,histological differences and clinical response to drugs in colon cancer and rectal cancer, can not only reduce the economic burden of patients,but also provide the most scientific basis for the precise treatment of patients gradually.
[Abstract] At present, more and more evidence shows that colon and rectal cancers are different diseases. There are many differences no matter in the epidemiology, anatomy and histology, molecular characteristics, transfer patterns, or clinical treatment methods, therapeutic effects and prognosis. In clinical treatment, it cann’t be considered as the same disease in general. Through the retrospective analysis of the three clinical studies of CALGB/SWOG 80405, CRYSTAL, and FIRE-3, it has been found that there were significant differences in the efficacy of cetuximab and bevacizumab in left and right colon cancer. Based on the above clinical trials, the National Cancer Institute for the United States (NCCN) for the first time includes the guidelines for the impact of primary sites on the treatment of colon cancer into guidelines in 2017. In the current era of advocating precision and individualized treatment, to clarify the pathogenesis,histological differences and clinical response to drugs in colon cancer and rectal cancer, can not only reduce the economic burden of patients,but also provide the most scientific basis for the precise treatment of patients gradually.
2018, 25(10):987-993.
DOI: 10.3872/j.issn.1007-385X.2018.10.003
Abstract:
Objective: To investigate whether inhibitor of differentiation 1 gene (Id1) and Id3 gene can synergistically promote epithelial-mesenchymal transition (EMT), invasion and migration of colon cancer SW620 cells and to explore its underlying mechanisms.Methods: The SW620 cell strain with Idl or Id3 gene knockdown and the SW620 cell strain with Id1/Id3 gene double-knockdown were constructed by lentiviral vectors transfection. The SW620 cells were divided into four groups, which included SW620-Sh-Id1 group (transfected with shRNA-Id1), SW620-Sh-Id3 group (transfected with shRNA-Id3), SW620-Sh-Id1-Id3 group (transfected with shRNAId1 plus shRNA-Id3) and SW620-NC group (transfected with negative lentivirus). The efficiency of knockdown was detected by Realtime qPCR and Western blotting. The influence of stable knockdown of Idl or Id3 on cell morphological change was observed under a microscope. The changes of migration and invasion abilities of the SW620 cells were determined by wound healing assay and Transwell assay. EMT, invasion and migration related proteins were measured by Western blotting. Results: The SW620 cell strains with Idl and/or Id3 gene knockdown were successfully constructed. Idl and Id3 knockdown induced the epithelial-like to the mesenchymanl-like transformation of SW620 cells. (1) Compared with the control group, the invasion and migration abilities of the SW620 cells were significantly decreased in the SW620-Sh-Id1 group and SW620-Sh-Id3 group (all P<0.05). (2) Meanwhile, the invasion and migration abilities in the SW620-Sh-Id1-Id3 group were obviously weaker than the SW620-Sh-Id1 group and SW620-Sh-Id3 group (all P<0.05). (3)Compared with the control group, the SW620-Sh-Id1 group and SW620-Sh-Id3 group had a reduction in the protein expressions of β-catenin, snail1 and MMP2, and an increase in the protein expressions of E-cadherin and TIMP2 (all P<0.05). (4) Compared with the SW620-Sh-Id1 group and SW620-Sh-Id3 group , the protein expressions of β-catenin, snail1 and MMP2 were reduced, and the protein expressions of E-cadherin and TIMP2 were increased in the SW620-Sh-Id1-Id3 group (all P<0.05). Conclusion: Id1 and Id3 could synergistically influence invasion and migration of SW620 cells, possibly through inducing EMT.
Objective: To investigate whether inhibitor of differentiation 1 gene (Id1) and Id3 gene can synergistically promote epithelial-mesenchymal transition (EMT), invasion and migration of colon cancer SW620 cells and to explore its underlying mechanisms.Methods: The SW620 cell strain with Idl or Id3 gene knockdown and the SW620 cell strain with Id1/Id3 gene double-knockdown were constructed by lentiviral vectors transfection. The SW620 cells were divided into four groups, which included SW620-Sh-Id1 group (transfected with shRNA-Id1), SW620-Sh-Id3 group (transfected with shRNA-Id3), SW620-Sh-Id1-Id3 group (transfected with shRNAId1 plus shRNA-Id3) and SW620-NC group (transfected with negative lentivirus). The efficiency of knockdown was detected by Realtime qPCR and Western blotting. The influence of stable knockdown of Idl or Id3 on cell morphological change was observed under a microscope. The changes of migration and invasion abilities of the SW620 cells were determined by wound healing assay and Transwell assay. EMT, invasion and migration related proteins were measured by Western blotting. Results: The SW620 cell strains with Idl and/or Id3 gene knockdown were successfully constructed. Idl and Id3 knockdown induced the epithelial-like to the mesenchymanl-like transformation of SW620 cells. (1) Compared with the control group, the invasion and migration abilities of the SW620 cells were significantly decreased in the SW620-Sh-Id1 group and SW620-Sh-Id3 group (all P<0.05). (2) Meanwhile, the invasion and migration abilities in the SW620-Sh-Id1-Id3 group were obviously weaker than the SW620-Sh-Id1 group and SW620-Sh-Id3 group (all P<0.05). (3)Compared with the control group, the SW620-Sh-Id1 group and SW620-Sh-Id3 group had a reduction in the protein expressions of β-catenin, snail1 and MMP2, and an increase in the protein expressions of E-cadherin and TIMP2 (all P<0.05). (4) Compared with the SW620-Sh-Id1 group and SW620-Sh-Id3 group , the protein expressions of β-catenin, snail1 and MMP2 were reduced, and the protein expressions of E-cadherin and TIMP2 were increased in the SW620-Sh-Id1-Id3 group (all P<0.05). Conclusion: Id1 and Id3 could synergistically influence invasion and migration of SW620 cells, possibly through inducing EMT.
2018, 25(10):994-998.
DOI: 10.3872/j.issn.1007-385X.2018.10.004
Abstract:
Objective: To explore the effect of histone deacetylase (HDAC) inhibitor valproic acid (VPA) on the epithelial-mesenchymal transition (EMT) of colon cancer. Methods: With four colon carcinoma cell lines (DLD-1, HCT116, SW480 and HT29) as study subjects, the effect of different concentrations of VPA (0.5，5 mmol/L) on cell proliferation was detected by MTT assay. The expression level of EMT-related proteins (E-cadherin and vimentin) was detected by Western blotting; Phenotypic changes of E-cadherin and vimentin were detected by immunofluorescence staining; Cell migration and invasion ability was detected by wound healing and Transwell invasion assay, respectively. Results: After treated with different concentrations of VPA for 48 h, low concentration of VPA merely exerted any effect on the cell proliferation rate of four colon cancer cell lines, and thus was chosen as the experiment concentration;The results of Western blotting showed that the expression of E-cadherin was reduced (P<0.05) and vimentin was increased (P<0.05) in colon carcinoma cells by VPA treatment (0.5 mmol/L); Immunofluorescence staining revealed membranous attenuation or nuclear translocation of E-cadherin and enhanced expression of vimentin after VPA treatment (0.5 mmol/L), and these responses occurred after 6 h and sustained until 24 h; Wound healing and Transwell invasion assay showed increased migration and invasion ability following VPA treatment (0.5 mmol/L). Conclusion: Low concentration VPA could induce the development of EMT in colon cancer cells by nuclear translocation of E-cadherin, and obviously enhance the migration and invasion ability of colon cancer cells; Thus, HDAC inhibitors, as a new type anti-cancer option, shall be carefully considered before their application in colon cancer.
Objective: To explore the effect of histone deacetylase (HDAC) inhibitor valproic acid (VPA) on the epithelial-mesenchymal transition (EMT) of colon cancer. Methods: With four colon carcinoma cell lines (DLD-1, HCT116, SW480 and HT29) as study subjects, the effect of different concentrations of VPA (0.5，5 mmol/L) on cell proliferation was detected by MTT assay. The expression level of EMT-related proteins (E-cadherin and vimentin) was detected by Western blotting; Phenotypic changes of E-cadherin and vimentin were detected by immunofluorescence staining; Cell migration and invasion ability was detected by wound healing and Transwell invasion assay, respectively. Results: After treated with different concentrations of VPA for 48 h, low concentration of VPA merely exerted any effect on the cell proliferation rate of four colon cancer cell lines, and thus was chosen as the experiment concentration;The results of Western blotting showed that the expression of E-cadherin was reduced (P<0.05) and vimentin was increased (P<0.05) in colon carcinoma cells by VPA treatment (0.5 mmol/L); Immunofluorescence staining revealed membranous attenuation or nuclear translocation of E-cadherin and enhanced expression of vimentin after VPA treatment (0.5 mmol/L), and these responses occurred after 6 h and sustained until 24 h; Wound healing and Transwell invasion assay showed increased migration and invasion ability following VPA treatment (0.5 mmol/L). Conclusion: Low concentration VPA could induce the development of EMT in colon cancer cells by nuclear translocation of E-cadherin, and obviously enhance the migration and invasion ability of colon cancer cells; Thus, HDAC inhibitors, as a new type anti-cancer option, shall be carefully considered before their application in colon cancer.
5 PD-1 antibody enhanced anti-tumor efficacy of oxaliplatin against colon cancer in vitro and in vivo
2018, 25(10):999-1005.
DOI: 10.3872/j.issn.1007-385X.2018.10.005
Abstract:
Objective: To explore the anti-tumor effects of oxaliplatin (OXA) combined with PD-1 antibody on colon cancer. Methods:Flow cytometry was used to detect the expression of PD-L1 in colon cancer cell lines HCT-116 and HT-29. Co-culture method was used to detect the secretion of cytokines and the changes of CD4/CD8 subsets in T-cells that co-cultured with HCT-116 cells, which were pretreated with OXA in combination with/without PD-1 antibody; The CT26 transplanted tumor model of colon cancer in BALB/c mice was established and treated with the combination of OXA and PD-1 to evaluate their anti-tumor efficacy. Meanwhile, CD8 antibody was used to scavenge CD8+ T cells in mice, and to evaluate the role of CD8+ T cells in the anti-tumor effect of OXA in vivo. Results:OXA could significantly increase the expression of PD-L1 on the surface of colon cancer cells. Compared with pure T-cells, the T cells co-cultured with colon cancer HCT-116 cells that pre-treated by OXA, exhibited significantly reduced IL-2, IFN-γ and TNF levels (all P<0.05) in its culture supernatant and decreased ratio of CD4+ memory T cell / CD8+TEMER (P<0.05), whereas there was increased cell proportion of the CD4+ (P>0.05) and CD8+ (P<0.05) na?ve T cells. After co-treated with PD-1 antibody, compared with the single treatment of OXA, IFN-γ and IL-10 content (P<0.05) in culture supernatant and the subsets of CD8+ TCM and TEMRA ratio (P>0.05) were increased. In vivo experiments showed that OXA combined with PD-1 antibody could enhance its anti-tumor activity, the tumor suppression rates were 25.6% (OXA) and 29.1% (αPD-1), respectively, however, the rate of tumor inhibition was increased to 58.2% when combined (P<0.05, compared to OXA or αPD-1 group). After scavenging CD8+ T cells in mice, the antitumor activity of OXA dropped from 68.4% to 46.2% (P<0.05). Conclusion: OXA combined with PD-1 antibody had synergistic anti-tumor effect, and CD8+ T cells played an important role in the antitumor activity of OXA.
Objective: To explore the anti-tumor effects of oxaliplatin (OXA) combined with PD-1 antibody on colon cancer. Methods:Flow cytometry was used to detect the expression of PD-L1 in colon cancer cell lines HCT-116 and HT-29. Co-culture method was used to detect the secretion of cytokines and the changes of CD4/CD8 subsets in T-cells that co-cultured with HCT-116 cells, which were pretreated with OXA in combination with/without PD-1 antibody; The CT26 transplanted tumor model of colon cancer in BALB/c mice was established and treated with the combination of OXA and PD-1 to evaluate their anti-tumor efficacy. Meanwhile, CD8 antibody was used to scavenge CD8+ T cells in mice, and to evaluate the role of CD8+ T cells in the anti-tumor effect of OXA in vivo. Results:OXA could significantly increase the expression of PD-L1 on the surface of colon cancer cells. Compared with pure T-cells, the T cells co-cultured with colon cancer HCT-116 cells that pre-treated by OXA, exhibited significantly reduced IL-2, IFN-γ and TNF levels (all P<0.05) in its culture supernatant and decreased ratio of CD4+ memory T cell / CD8+TEMER (P<0.05), whereas there was increased cell proportion of the CD4+ (P>0.05) and CD8+ (P<0.05) na?ve T cells. After co-treated with PD-1 antibody, compared with the single treatment of OXA, IFN-γ and IL-10 content (P<0.05) in culture supernatant and the subsets of CD8+ TCM and TEMRA ratio (P>0.05) were increased. In vivo experiments showed that OXA combined with PD-1 antibody could enhance its anti-tumor activity, the tumor suppression rates were 25.6% (OXA) and 29.1% (αPD-1), respectively, however, the rate of tumor inhibition was increased to 58.2% when combined (P<0.05, compared to OXA or αPD-1 group). After scavenging CD8+ T cells in mice, the antitumor activity of OXA dropped from 68.4% to 46.2% (P<0.05). Conclusion: OXA combined with PD-1 antibody had synergistic anti-tumor effect, and CD8+ T cells played an important role in the antitumor activity of OXA.
2018, 25(10):1006-1012.
DOI: 10.3872/j.issn.1007-385X.2018.10.006
Abstract:
Objective: To investigate the effects and mechanisms of miR-126-5p on proliferation, migration, invasion and apoptosis of colon cancer SW480 cells. Methods: Cells were transferred with miR-126 mimic and pcDNA Notch2 (pc-Notch2) respectively or simultaneously.Real-time fluorescence quantitative PCR was performed to detect the expression of miR-126 and Notch2. The relationship of miR-126-5p and Notch2 was determined by luciferase reporter assay. The CCK-8 assay, wound healing assay, Transwell and flow cytometry were performed to examine cell proliferation, migration, invasion and apoptosis, respectively. The protein levels of Notch2, proliferating cell nuclear antigen (PCNA), cleaved Caspase-3, metalloproteinase-2 (MMP-2) and MMP-9 were measured by Western blotting. Results: miR-126 mimic significantly increased expression level of miR-126-5p but reduced the expression of Notch2 in SW480 cells (all P<0.01); in the meanwhile, a binding site with miR-126-5p was confirmed on Notch2. Up-regulating the expression of miR-126-5p inhibited cell proliferation and the expression of PCNA (P<0.01), increased the cell apoptosis rate and protein level of cleaved Caspase-3 notably (all P<0.01). Pc-Notch2 obviously alleviated the effects of miR-126 mimic on cell proliferation and apoptosis (all P<0.01). Furthermore, miR-126 mimic significantly decreased the wound healing rate and invasive cell numbers (all P<0.01),and down-regulated the expressions of MMP-2 and MMP-9 (P<0.01); pc-Notch2 alleviated the effects of miR-126 mimic on cell migration,invasion and the expressions of MMP-2 and MMP-9 (all P<0.01). Conclusion: miR-126-5p can attenuate proliferation, migration and invasive ability of colon SW480 cells via inhibiting the expression of Notch2.
Objective: To investigate the effects and mechanisms of miR-126-5p on proliferation, migration, invasion and apoptosis of colon cancer SW480 cells. Methods: Cells were transferred with miR-126 mimic and pcDNA Notch2 (pc-Notch2) respectively or simultaneously.Real-time fluorescence quantitative PCR was performed to detect the expression of miR-126 and Notch2. The relationship of miR-126-5p and Notch2 was determined by luciferase reporter assay. The CCK-8 assay, wound healing assay, Transwell and flow cytometry were performed to examine cell proliferation, migration, invasion and apoptosis, respectively. The protein levels of Notch2, proliferating cell nuclear antigen (PCNA), cleaved Caspase-3, metalloproteinase-2 (MMP-2) and MMP-9 were measured by Western blotting. Results: miR-126 mimic significantly increased expression level of miR-126-5p but reduced the expression of Notch2 in SW480 cells (all P<0.01); in the meanwhile, a binding site with miR-126-5p was confirmed on Notch2. Up-regulating the expression of miR-126-5p inhibited cell proliferation and the expression of PCNA (P<0.01), increased the cell apoptosis rate and protein level of cleaved Caspase-3 notably (all P<0.01). Pc-Notch2 obviously alleviated the effects of miR-126 mimic on cell proliferation and apoptosis (all P<0.01). Furthermore, miR-126 mimic significantly decreased the wound healing rate and invasive cell numbers (all P<0.01),and down-regulated the expressions of MMP-2 and MMP-9 (P<0.01); pc-Notch2 alleviated the effects of miR-126 mimic on cell migration,invasion and the expressions of MMP-2 and MMP-9 (all P<0.01). Conclusion: miR-126-5p can attenuate proliferation, migration and invasive ability of colon SW480 cells via inhibiting the expression of Notch2.
2018, 25(10):1013-1020.
DOI: 10.3872/j.issn.1007-385X.2018.10.007
Abstract:
Objective: To investigate the mechanism of miR-31-5p/tension protein 1 gene (TNS1) axis modulating radiotherapy resistance in breast cancer. Methods: The breast cancer tissues and corresponding para-cancerous tissues of 21 patients with breast cancer,who underwent surgical resection at Department of Cancer Radiotherapy of Nanyang Central Hospital from July 2017 to December 2017, were collected for this study; breast cancer cell lines (MCF-7，MDA-MB-23 and SKBR-3) were also collected; qPCR was applied to detect the expression level of miR-31-5p in breast cancer tissues and cell lines. The radiation resistant cell line MCF-7R was constructed by using 6 MV-X ray radiotherapy treatment. Subsequently, the influence of over-expression/kockdown of miR-31-5p on radiation sensitivity of MCF-7 and MCF-7R cells were detected by colony formation assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Moreover, luciferase reporter assay was used to verify whether TNS1 was a target gene of miR-31-5p. Results: Compared with para-cancerous tissues, normal mammary epithelial MCF-10A cells and MCF-7 cells, miR-31-5p was low-expressed in breast cancer, cell lines and MCF-7R (all P<0.01). Over-expression of miR-31-5p resulted in inhibited invasion and promoted apoptosis of MCF-7R cells (P<0.01), whereas miR-31-5p knockdown got opposite results in MCF-7 cells. Moreover, luciferase reporter assay confirmed that TNS1 was a target gene of miR-31-5p. Over-expression of miR-31-5p inhibited invasion and increased radio-sensitivity, apoptosis of MCF-7R cell via targeting TNS1 (P<0.01), whereas knockdown of miR-31-5p significantly promoted the invasion but reduced apoptosis of MCF-7R cells (all P<0.01), and further up-regulated the radio-sensitivity of MCF-7R cells.Conclusion: miR-31-5p/TNS1 axis regulates the radiotherapy resistance of breast cancer, and over-expression of miR-31-5p may reverse the resistance of MCF-7R to radiotherapy.
Objective: To investigate the mechanism of miR-31-5p/tension protein 1 gene (TNS1) axis modulating radiotherapy resistance in breast cancer. Methods: The breast cancer tissues and corresponding para-cancerous tissues of 21 patients with breast cancer,who underwent surgical resection at Department of Cancer Radiotherapy of Nanyang Central Hospital from July 2017 to December 2017, were collected for this study; breast cancer cell lines (MCF-7，MDA-MB-23 and SKBR-3) were also collected; qPCR was applied to detect the expression level of miR-31-5p in breast cancer tissues and cell lines. The radiation resistant cell line MCF-7R was constructed by using 6 MV-X ray radiotherapy treatment. Subsequently, the influence of over-expression/kockdown of miR-31-5p on radiation sensitivity of MCF-7 and MCF-7R cells were detected by colony formation assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Moreover, luciferase reporter assay was used to verify whether TNS1 was a target gene of miR-31-5p. Results: Compared with para-cancerous tissues, normal mammary epithelial MCF-10A cells and MCF-7 cells, miR-31-5p was low-expressed in breast cancer, cell lines and MCF-7R (all P<0.01). Over-expression of miR-31-5p resulted in inhibited invasion and promoted apoptosis of MCF-7R cells (P<0.01), whereas miR-31-5p knockdown got opposite results in MCF-7 cells. Moreover, luciferase reporter assay confirmed that TNS1 was a target gene of miR-31-5p. Over-expression of miR-31-5p inhibited invasion and increased radio-sensitivity, apoptosis of MCF-7R cell via targeting TNS1 (P<0.01), whereas knockdown of miR-31-5p significantly promoted the invasion but reduced apoptosis of MCF-7R cells (all P<0.01), and further up-regulated the radio-sensitivity of MCF-7R cells.Conclusion: miR-31-5p/TNS1 axis regulates the radiotherapy resistance of breast cancer, and over-expression of miR-31-5p may reverse the resistance of MCF-7R to radiotherapy.
2018, 25(10):1021-1025.
DOI: 10.3872/j.issn.1007-385X.2018.10.008
Abstract:
Objective: To validate the effect and the possible mechanism of human regulatory factor X1 (RFX1) over-expression on the proliferation and invasion of glioma F98 cells. Methods: RFX1-overexpressed F98 cells (F98-RFX1 group) were constructed by lentivirus transfection, a control group (F98-Vector group) and normal group (F98 group) were established. The effect of RFX1 over-expression on F98 cell proliferation was observed with counting method, cell apoptosis was determined by AnnexinV-PI staining, and the cell invasion was observed with Transwell method. Results: F98 cell line over-expressing RFX1 was successfully established. The proliferation capacity of F98-RFX1 group was significantly lower than that of F98 group (48 h: [12.08±2.17]×104/ml vs [23.67±4.51]×104/ml, P<0.05] and F98-Vector group (96 h: [8.17±0.31]×104 /ml vs [18.58±1.18]×104 /ml, P<0.05); The apoptosis level of cells in F98-RFX1 group was significantly increased ([21.89±2.33]% vs [3.38±1.39]%, [10.42±1.83]%, P<0.05]; The invasiveness of cells in F98-RFX1 group was significantly reduced ([33.3±7.99] vs [56.5±13.9], [60.6±11.8], P<0.01). Conclusion: RFX1 can regulate the expression of genes related with proliferation and invasion, thereby inhibiting the proliferation and invasion ability of glioma cells and promote cell apoptosis.
Objective: To validate the effect and the possible mechanism of human regulatory factor X1 (RFX1) over-expression on the proliferation and invasion of glioma F98 cells. Methods: RFX1-overexpressed F98 cells (F98-RFX1 group) were constructed by lentivirus transfection, a control group (F98-Vector group) and normal group (F98 group) were established. The effect of RFX1 over-expression on F98 cell proliferation was observed with counting method, cell apoptosis was determined by AnnexinV-PI staining, and the cell invasion was observed with Transwell method. Results: F98 cell line over-expressing RFX1 was successfully established. The proliferation capacity of F98-RFX1 group was significantly lower than that of F98 group (48 h: [12.08±2.17]×104/ml vs [23.67±4.51]×104/ml, P<0.05] and F98-Vector group (96 h: [8.17±0.31]×104 /ml vs [18.58±1.18]×104 /ml, P<0.05); The apoptosis level of cells in F98-RFX1 group was significantly increased ([21.89±2.33]% vs [3.38±1.39]%, [10.42±1.83]%, P<0.05]; The invasiveness of cells in F98-RFX1 group was significantly reduced ([33.3±7.99] vs [56.5±13.9], [60.6±11.8], P<0.01). Conclusion: RFX1 can regulate the expression of genes related with proliferation and invasion, thereby inhibiting the proliferation and invasion ability of glioma cells and promote cell apoptosis.
ZHANG Zezhong
,
JIA Yulin
,
QILGER Bao
,
FANG Yi
,
LI Chunhui
,
LI Jianlei
,
GU Ye
,
DENG Zixin
,
ZHANG Haiping
,
MA Wei
2018, 25(10):1026-1033.
DOI: 10.3872/j.issn.1007-385X.2018.10.009
Abstract:
Objective: The present study was aimed to explore the role and distinctive mechanism of SPIDR, the key regulatory protein of homologous recombination pathway, in progression of small cell lung cancer (SCLC). Methods: 60 SCLC specimens and 44 normal lung tissues were collected from the patients undergoing tumor resection and bronchoscopic puncture in Shanghai Pulmonary Hospital Affiliated to Tongji University from January 2013 to January 2015. The expression of SPIDR in clinical samples and NCIH446 (SCLC cell line) and MRC-5 (normal cell line) were assayed by Real-time PCR. The role of SPIDR in SCLC was investigated in vivo and in vitro by the expression of SPIDR were artificially modified in NCI-H446. Results: Smoking was significantly associated with the occurrence of SCLC (P<0.01). The expression of SPIDR mRNA in SCLC tissues was lower than that of normal lung tissues (P<0.01), and the SPIDR transcriptional and translational levels of NCI-H446 cells were also lower than that of MRC-5. Although there is no significant changes of cell growth rate and susceptibility to cisplatin and etoposide in the NCI-H446 cells overexpressing SPIDR.However, the volume of xenograft tumors of overexpressed SPIDR group decreased by 58.99% (P<0.01) and 61.84% (P<0.01) than that of the original NCI-H446 cells and the NCI-H446 cells transfected with vector (pMSCV) and the average tumor mass decreased by 61.70% (P<0.01) and 70.25% (P<0.01) respectively. When the fetal bovine serum content in the medium was reduced to 3%, the growth rate of NCI-H446 cells overexpressing SPIDR was 22.33% (P<0.01) and 20.24% (P<0.05) lower than that of the original NCIH446 cells and control group, the similar results were obtained from the 1% serum concentration experiment as well. Conclusion: The expression of SPIDR, the key regulatory protein in the DNA double strand break homologous recombination repair pathway, was significantly suppressed in SCLC tissues, which markedly accelerated the growth of NCI-H446 cells in vivo and reduced the reliance of NCIH446 cells to the serum. The detailed mechanism is worthy of further investigation.
Objective: The present study was aimed to explore the role and distinctive mechanism of SPIDR, the key regulatory protein of homologous recombination pathway, in progression of small cell lung cancer (SCLC). Methods: 60 SCLC specimens and 44 normal lung tissues were collected from the patients undergoing tumor resection and bronchoscopic puncture in Shanghai Pulmonary Hospital Affiliated to Tongji University from January 2013 to January 2015. The expression of SPIDR in clinical samples and NCIH446 (SCLC cell line) and MRC-5 (normal cell line) were assayed by Real-time PCR. The role of SPIDR in SCLC was investigated in vivo and in vitro by the expression of SPIDR were artificially modified in NCI-H446. Results: Smoking was significantly associated with the occurrence of SCLC (P<0.01). The expression of SPIDR mRNA in SCLC tissues was lower than that of normal lung tissues (P<0.01), and the SPIDR transcriptional and translational levels of NCI-H446 cells were also lower than that of MRC-5. Although there is no significant changes of cell growth rate and susceptibility to cisplatin and etoposide in the NCI-H446 cells overexpressing SPIDR.However, the volume of xenograft tumors of overexpressed SPIDR group decreased by 58.99% (P<0.01) and 61.84% (P<0.01) than that of the original NCI-H446 cells and the NCI-H446 cells transfected with vector (pMSCV) and the average tumor mass decreased by 61.70% (P<0.01) and 70.25% (P<0.01) respectively. When the fetal bovine serum content in the medium was reduced to 3%, the growth rate of NCI-H446 cells overexpressing SPIDR was 22.33% (P<0.01) and 20.24% (P<0.05) lower than that of the original NCIH446 cells and control group, the similar results were obtained from the 1% serum concentration experiment as well. Conclusion: The expression of SPIDR, the key regulatory protein in the DNA double strand break homologous recombination repair pathway, was significantly suppressed in SCLC tissues, which markedly accelerated the growth of NCI-H446 cells in vivo and reduced the reliance of NCIH446 cells to the serum. The detailed mechanism is worthy of further investigation.
2018, 25(10):1034-1041.
DOI: 10.3872/j.issn.1007-385X.2018.10.010
Abstract:
Objective: To explore the role and molecular mechanism of high intensity focused ultrasound (HIFU) inhibits pancreatic cancer cell proliferation and invasion via regulating miR-1297/PTEN axis. Methods: With treating the cells with HIFU for 1 to 3 seconds,the effect of HIFU on cell proliferation, invasion and apoptosis of PANC-1 cells in vitro was examined by CCK-8, Transwell and Annexin V-FITC/PI double staining flow cytometry, respectively. The effect of HIFU on expression of miR-1297 and PTEN were measured by qPCR and Western blotting. Moreover, the relationship between miR-1297 and PTEN was examined by dual luciferase report assay. Western blotting was used to detect the effect of HIFU on the expression of Akt, p-Akt (308) and p-Akt (473) after transfected with miR-1297 inhibitor and PTEN-siRNA. Results: HIFU treatment significantly inhibited the cell proliferation, invasion and promoted apoptosis of PANC-1 cells (all P<0.01), which was associated with inhibition of miR-1297 expression and activation of PTEN expression in pancreatic cancer cells (all P<0.01). Moreover, miR-1297 directly binds to the 3′ UTR of PTEN mRNA to suppress its expression in PANC-1 cells. Further, HIFU exposure could significantly inhibit the expression of the phosphorylation of Akt (P<0.01).Conclusion: HIFU inhibits PTEN and blocks Akt signaling by down-regulating miR-1297, thereby suppresses the occurrence and progress of pancreatic cancer.
Objective: To explore the role and molecular mechanism of high intensity focused ultrasound (HIFU) inhibits pancreatic cancer cell proliferation and invasion via regulating miR-1297/PTEN axis. Methods: With treating the cells with HIFU for 1 to 3 seconds,the effect of HIFU on cell proliferation, invasion and apoptosis of PANC-1 cells in vitro was examined by CCK-8, Transwell and Annexin V-FITC/PI double staining flow cytometry, respectively. The effect of HIFU on expression of miR-1297 and PTEN were measured by qPCR and Western blotting. Moreover, the relationship between miR-1297 and PTEN was examined by dual luciferase report assay. Western blotting was used to detect the effect of HIFU on the expression of Akt, p-Akt (308) and p-Akt (473) after transfected with miR-1297 inhibitor and PTEN-siRNA. Results: HIFU treatment significantly inhibited the cell proliferation, invasion and promoted apoptosis of PANC-1 cells (all P<0.01), which was associated with inhibition of miR-1297 expression and activation of PTEN expression in pancreatic cancer cells (all P<0.01). Moreover, miR-1297 directly binds to the 3′ UTR of PTEN mRNA to suppress its expression in PANC-1 cells. Further, HIFU exposure could significantly inhibit the expression of the phosphorylation of Akt (P<0.01).Conclusion: HIFU inhibits PTEN and blocks Akt signaling by down-regulating miR-1297, thereby suppresses the occurrence and progress of pancreatic cancer.
2018, 25(10):1042-1047.
DOI: 10.3872/j.issn.1007-385X.2018.10.011
Abstract:
Objective: To explore the expression of long non-coding RNA RP11-259P1.1 (lncRNA RP11-259P1.1) in small cell lung cancer (SCLC) tissues and to analyze the relationship between lncRNA RP11-259P1.1 expression and SCLC clinicopathological characteristics,as well as to investigate its effect in chemoresistance. Methods: Tissue samples, including 158 cases of tumor tissues from SCLC patients, who underwent bronchoscopic biopsy, puncture biopsy and surgical resection, 48 cases of para-cancerous tissues and 40 cases of normal lung tissues, collected from January 2012 to December 2016 in the Sixth People’s Hospital of Chengdu and General Hospital of Chengdu Military Region，were used in this study. The expression of lncRNA RP11-259P1.1 was detected by Real-time fluorescence quantitative PCR (qPCR). χ2 test was used to analyze the relationship between the expression of lncRNA RP11-259P1.1 and the clinicopathological characteristics as well as chemotherapeutic resistance in SCLC patients. Relationship between lncRNA RP11-259P1.1 expression and prognosis of SCLC patients was analyzed by univariate and multivariate Cox regression analysis. Results: The expression of lncRNA RP11-259P1.1 in SCLC tissues was significantly higher than that in para-cancerous tissues and normal lung tissues (all P < 0.01). The expression of lncRNA RP11-259P1.1 in cancer tissues of chemosensitive group was significantly lower than that of chemoresistant group (P<0.05). The expression of lncRNA RP11-259P 1.1 was not correlated with gender and age, but significantly correlated with tumor stage, metastasis and chemosensitivity (all P<0.05). PFS and OS in patients with high lncRNA RP11-259P 1.1 expression were significantly shorter than those in patients with low expression ([12.25±1.83] vs [22.29±1.58] months, [23.55±1.35]vs [31.75±2.43] months, all P<0.01). The expression of lncRNA RP11-259P 1.1, tumor stage and distant metastasis were the independent prognostic factors in SCLC patients (all P<0.05). Conclusion: The high expression of lncRNA RP11-259P1.1 in SCLC tissues is associated with chemosensitivity and prognosis of SCLC patients, and may be a potential biomarker for prognosis evaluation in SCLC patients.
Objective: To explore the expression of long non-coding RNA RP11-259P1.1 (lncRNA RP11-259P1.1) in small cell lung cancer (SCLC) tissues and to analyze the relationship between lncRNA RP11-259P1.1 expression and SCLC clinicopathological characteristics,as well as to investigate its effect in chemoresistance. Methods: Tissue samples, including 158 cases of tumor tissues from SCLC patients, who underwent bronchoscopic biopsy, puncture biopsy and surgical resection, 48 cases of para-cancerous tissues and 40 cases of normal lung tissues, collected from January 2012 to December 2016 in the Sixth People’s Hospital of Chengdu and General Hospital of Chengdu Military Region，were used in this study. The expression of lncRNA RP11-259P1.1 was detected by Real-time fluorescence quantitative PCR (qPCR). χ2 test was used to analyze the relationship between the expression of lncRNA RP11-259P1.1 and the clinicopathological characteristics as well as chemotherapeutic resistance in SCLC patients. Relationship between lncRNA RP11-259P1.1 expression and prognosis of SCLC patients was analyzed by univariate and multivariate Cox regression analysis. Results: The expression of lncRNA RP11-259P1.1 in SCLC tissues was significantly higher than that in para-cancerous tissues and normal lung tissues (all P < 0.01). The expression of lncRNA RP11-259P1.1 in cancer tissues of chemosensitive group was significantly lower than that of chemoresistant group (P<0.05). The expression of lncRNA RP11-259P 1.1 was not correlated with gender and age, but significantly correlated with tumor stage, metastasis and chemosensitivity (all P<0.05). PFS and OS in patients with high lncRNA RP11-259P 1.1 expression were significantly shorter than those in patients with low expression ([12.25±1.83] vs [22.29±1.58] months, [23.55±1.35]vs [31.75±2.43] months, all P<0.01). The expression of lncRNA RP11-259P 1.1, tumor stage and distant metastasis were the independent prognostic factors in SCLC patients (all P<0.05). Conclusion: The high expression of lncRNA RP11-259P1.1 in SCLC tissues is associated with chemosensitivity and prognosis of SCLC patients, and may be a potential biomarker for prognosis evaluation in SCLC patients.
2018, 25(10):1048-1054.
DOI: 10.3872/j.issn.1007-385X.2018.10.012
Abstract:
Objective: To investigate the expression of galectin-3 protein in human breast cancer tissues and the effect of silencing galectin-3 gene on the migration, invasion and apoptosis of human breast cancer MCF-7 cells. Methods: The relative expression of galectin-3 protein in 15 cases of breast cancer tissues and corresponding para-cancerous tissues were detected by Western blotting; The expression of galectin-3 protein in paraffin sections of 100 cases of breast cancer tissues were detected by immunohistochemistry, and the correlation between galectin-3 expression and the clinicopathological characteristics of breast cancer patients was also analyzed. Galectin-3 siRNA were transfected into human breast cancer MCF-7 cells by liposome, then Real-time PCR and Western blotting were used to detect the mRNA and protein expression of galectin-3. The effect of galectin-3 gene silencing on cell migration and invasion ability of MCF-7 cells were detected by Transwell method. The effect of galectin-3 gene silencing on apoptosis of MCF-7 cells were detected by flow cytometry. Results: Western blotting detection showed that the relative expression of galectin-3 protein in breast cancer tissues were significantly higher than that in para-cancerous tissues (P<0.05);Immunohistochemistry detection showed that the positive expression rate of galectin-3 protein in breast cancer tissues was 67.00%, the positive expression rates in the lymph node metastasis, hormone receptor (ER, PR) negative groups were significantly higher (P<0.05), and the positive expression rate of galectin-3 protein were increased with the increase of TNM stage and histological grade (P<0.05); Galectin-3 siRNA transfection could significantly reduce the mRNA and protein expression of galectin-3 in MCF-7 cells (P<0.05), and reduce the invasion and migration ability but significantly improve the rate of apoptosis of MCF-7 cells (P<0.05). Conclusion: Galectin-3 is highly expressed in breast cancer tissues, and its silence can inhibit the invasion and metastasis of MCF-7 cells and induce apoptosis of MCF-7 cells. Galectin-3 can be used as a new target for biological therapy of breast cancer.
Objective: To investigate the expression of galectin-3 protein in human breast cancer tissues and the effect of silencing galectin-3 gene on the migration, invasion and apoptosis of human breast cancer MCF-7 cells. Methods: The relative expression of galectin-3 protein in 15 cases of breast cancer tissues and corresponding para-cancerous tissues were detected by Western blotting; The expression of galectin-3 protein in paraffin sections of 100 cases of breast cancer tissues were detected by immunohistochemistry, and the correlation between galectin-3 expression and the clinicopathological characteristics of breast cancer patients was also analyzed. Galectin-3 siRNA were transfected into human breast cancer MCF-7 cells by liposome, then Real-time PCR and Western blotting were used to detect the mRNA and protein expression of galectin-3. The effect of galectin-3 gene silencing on cell migration and invasion ability of MCF-7 cells were detected by Transwell method. The effect of galectin-3 gene silencing on apoptosis of MCF-7 cells were detected by flow cytometry. Results: Western blotting detection showed that the relative expression of galectin-3 protein in breast cancer tissues were significantly higher than that in para-cancerous tissues (P<0.05);Immunohistochemistry detection showed that the positive expression rate of galectin-3 protein in breast cancer tissues was 67.00%, the positive expression rates in the lymph node metastasis, hormone receptor (ER, PR) negative groups were significantly higher (P<0.05), and the positive expression rate of galectin-3 protein were increased with the increase of TNM stage and histological grade (P<0.05); Galectin-3 siRNA transfection could significantly reduce the mRNA and protein expression of galectin-3 in MCF-7 cells (P<0.05), and reduce the invasion and migration ability but significantly improve the rate of apoptosis of MCF-7 cells (P<0.05). Conclusion: Galectin-3 is highly expressed in breast cancer tissues, and its silence can inhibit the invasion and metastasis of MCF-7 cells and induce apoptosis of MCF-7 cells. Galectin-3 can be used as a new target for biological therapy of breast cancer.
2018, 25(10):1055-1059.
DOI: 10.3872/j.issn.1007-385X.2018.10.013
Abstract:
Objective: To explore the relationship between monocyte-to-lymphocyte ratio (MLR) in peripheral blood of patients with pulmonary sarcomatoid carcinoma (PSC) and their clinicopathological features and prognosis, and to investigate its clinical significance.Methods: A retrospective analysis was carried out to analyze the complete case data of 80 patients with PSC from October 2010 to April 2017 in Tianjin Cancer Hospital (monocyte and lymphocyte counts of peripheral blood, clinicopathological features, and survival follow-up). The receiver operating curve (ROC) was used to determine the best cut-off value of MLR for the prediction of overall survival time (OS). The patients were divided into high MLR group and low MLR group. Kaplan-Meier method was used to calculate OS and draw survival curves. The Log-Rank test was used to compare the difference in OS between the two groups. The variables with statistical significance in univariate analysis were included into the COX risk regression model to verify and calculate thehazard ratio (HR)and 95% confidence interval (95%CI). Results: The absolute median values of monocytes and lymphocytes were 0.63×109 /L and 1.84×109/L, respectively. The best cut-off value of MLR is 0.44. Univariate analysis shows that MLR≥0.44 (P<0.01), no radical surgery (P<0.01), clinical stage Ⅲ+Ⅳ (P<0.01), tumor maximal diameter > 3 cm (P<0.01), and LDH>247 U /L (P<0.01) are the poor prognostic factors affecting overall survival. Multivariate analysis shows that MLR≥0.44（HR=3.554; 95%CI=1.671-6.125; P<0.01),and clinical stage Ⅲ+Ⅳ（HR=3.275; 95%CI=2.047-9.399; P<0.01) are the independent risk factors for the overall survival of PSC, and radical surgery is an independent protective factor affecting the overall survival of PSC（HR=0.360; 95%CI=0.195-0.848; P<0.01). Conclusion:High MLR is an independent risk factor for poor prognosis in patients with PSC.
Objective: To explore the relationship between monocyte-to-lymphocyte ratio (MLR) in peripheral blood of patients with pulmonary sarcomatoid carcinoma (PSC) and their clinicopathological features and prognosis, and to investigate its clinical significance.Methods: A retrospective analysis was carried out to analyze the complete case data of 80 patients with PSC from October 2010 to April 2017 in Tianjin Cancer Hospital (monocyte and lymphocyte counts of peripheral blood, clinicopathological features, and survival follow-up). The receiver operating curve (ROC) was used to determine the best cut-off value of MLR for the prediction of overall survival time (OS). The patients were divided into high MLR group and low MLR group. Kaplan-Meier method was used to calculate OS and draw survival curves. The Log-Rank test was used to compare the difference in OS between the two groups. The variables with statistical significance in univariate analysis were included into the COX risk regression model to verify and calculate thehazard ratio (HR)and 95% confidence interval (95%CI). Results: The absolute median values of monocytes and lymphocytes were 0.63×109 /L and 1.84×109/L, respectively. The best cut-off value of MLR is 0.44. Univariate analysis shows that MLR≥0.44 (P<0.01), no radical surgery (P<0.01), clinical stage Ⅲ+Ⅳ (P<0.01), tumor maximal diameter > 3 cm (P<0.01), and LDH>247 U /L (P<0.01) are the poor prognostic factors affecting overall survival. Multivariate analysis shows that MLR≥0.44（HR=3.554; 95%CI=1.671-6.125; P<0.01),and clinical stage Ⅲ+Ⅳ（HR=3.275; 95%CI=2.047-9.399; P<0.01) are the independent risk factors for the overall survival of PSC, and radical surgery is an independent protective factor affecting the overall survival of PSC（HR=0.360; 95%CI=0.195-0.848; P<0.01). Conclusion:High MLR is an independent risk factor for poor prognosis in patients with PSC.
2018, 25(10):1060-1063.
DOI: 10.3872/j.issn.1007-385X.2018.10.014
Abstract:
[摘要] 恶性肿瘤居中国各类疾病死因之首，发病率与病死率呈逐年上升趋势。近几年来靶向治疗已广泛应用于临床，显示出良好的抗肿瘤效果，新靶点的探索和鉴定在靶向药物研发过程中起着重要作用。E3 泛素连接酶斑点型锌指结构蛋白（speckletype POZ protein，SPOP）作为治疗选择的潜在靶点，能特异性识别底物，使底物发生泛素化降解，广泛参与机体内多种生理、病理过程。研究发现SPOP基因突变或表达水平改变，通过调控AR/ERG、Akt-mTORC1、Hedgehog/Gli2 等多种信号通路影响恶性肿瘤的发生发展，并与前列腺癌、肾癌、结直肠癌等多种恶性肿瘤细胞增殖及远处转移密切相关。目前，SPOP影响恶性肿瘤发生发展的相关研究为靶向治疗恶性肿瘤奠定了基础，综述SPOP在恶性肿瘤的最新进展对抗肿瘤研究具有重要的意义。
[摘要] 恶性肿瘤居中国各类疾病死因之首，发病率与病死率呈逐年上升趋势。近几年来靶向治疗已广泛应用于临床，显示出良好的抗肿瘤效果，新靶点的探索和鉴定在靶向药物研发过程中起着重要作用。E3 泛素连接酶斑点型锌指结构蛋白（speckletype POZ protein，SPOP）作为治疗选择的潜在靶点，能特异性识别底物，使底物发生泛素化降解，广泛参与机体内多种生理、病理过程。研究发现SPOP基因突变或表达水平改变，通过调控AR/ERG、Akt-mTORC1、Hedgehog/Gli2 等多种信号通路影响恶性肿瘤的发生发展，并与前列腺癌、肾癌、结直肠癌等多种恶性肿瘤细胞增殖及远处转移密切相关。目前，SPOP影响恶性肿瘤发生发展的相关研究为靶向治疗恶性肿瘤奠定了基础，综述SPOP在恶性肿瘤的最新进展对抗肿瘤研究具有重要的意义。
2018, 25(10):1064-1071.
DOI: 10.3872/j.issn.1007-385X.2018.10.015
Abstract:
[摘要] 微小RNA（microRNA，miRNA）是一种内源性的长度为18~25 个核苷酸的非编码RNA，通过与蛋白质编码基因的mRNA结合来发挥重要的基因调控作用，与恶性肿瘤的发生发展密切相关。miR-32 作为miRNA家族的重要成员，在不同肿瘤中表达水平存在明显差异，因其与恶性肿瘤的相关性及本身表达的正反作用双向性，在miRNA领域受到了更多的关注。近年来研究发现，miR-32 对恶性肿瘤细胞的增殖、迁移与侵袭、自噬和凋亡均有影响。此外，miR-32 与其上游靶基因、肿瘤代谢及临床诊断和治疗也有密切的关系。本文就miR-32 在恶性肿瘤发生发展中的作用及其机制、临床诊治中应用等最新研究进展作一综述。
[摘要] 微小RNA（microRNA，miRNA）是一种内源性的长度为18~25 个核苷酸的非编码RNA，通过与蛋白质编码基因的mRNA结合来发挥重要的基因调控作用，与恶性肿瘤的发生发展密切相关。miR-32 作为miRNA家族的重要成员，在不同肿瘤中表达水平存在明显差异，因其与恶性肿瘤的相关性及本身表达的正反作用双向性，在miRNA领域受到了更多的关注。近年来研究发现，miR-32 对恶性肿瘤细胞的增殖、迁移与侵袭、自噬和凋亡均有影响。此外，miR-32 与其上游靶基因、肿瘤代谢及临床诊断和治疗也有密切的关系。本文就miR-32 在恶性肿瘤发生发展中的作用及其机制、临床诊治中应用等最新研究进展作一综述。
16 The role and mechanism of long non-coding RNA in the occurrence and development of bladder cancer
2018, 25(10):1072-1076.
DOI: 10.3872/j.issn.1007-385X.2018.10.016
Abstract:
[摘要] 膀胱癌是泌尿系统器官中最常见的恶性肿瘤之一，其病因及发病机制尚不十分清楚，且其具有发病率高、恶性程度高以及术后易复发等特点，因此对其病因、发生发展的具体分子机制的研究及阐明，将有力地促进膀胱癌的诊断及治疗。长链非编码RNA（long non-coding RNA，lncRNA）是细胞中一类转录本长度超过200 个核苷酸的非编码RNA分子，占RNA总量的98%。lncRNA具有与mRNA相似的结构，经过转录后加工，也具有polyA 尾巴和启动子结构，但是由于序列中缺少开放阅读框，而不参与或很少参与蛋白质编码。近年来，随着二代测序技术的广泛应用，越来越多的研究发现lncRNA在多个层面上参与细胞分化和个体发育等重要生命活动过程的调控，并与人类的重大疾病尤其是肿瘤密切相关。相关的研究表明，lncRNA参与靶基因的表达调控，在肿瘤的发生发展中发挥着重要的作用。本文对lncRNA在膀胱癌方面的最新研究进展进行了文献综述。
[摘要] 膀胱癌是泌尿系统器官中最常见的恶性肿瘤之一，其病因及发病机制尚不十分清楚，且其具有发病率高、恶性程度高以及术后易复发等特点，因此对其病因、发生发展的具体分子机制的研究及阐明，将有力地促进膀胱癌的诊断及治疗。长链非编码RNA（long non-coding RNA，lncRNA）是细胞中一类转录本长度超过200 个核苷酸的非编码RNA分子，占RNA总量的98%。lncRNA具有与mRNA相似的结构，经过转录后加工，也具有polyA 尾巴和启动子结构，但是由于序列中缺少开放阅读框，而不参与或很少参与蛋白质编码。近年来，随着二代测序技术的广泛应用，越来越多的研究发现lncRNA在多个层面上参与细胞分化和个体发育等重要生命活动过程的调控，并与人类的重大疾病尤其是肿瘤密切相关。相关的研究表明，lncRNA参与靶基因的表达调控，在肿瘤的发生发展中发挥着重要的作用。本文对lncRNA在膀胱癌方面的最新研究进展进行了文献综述。
2018, 25(10):1077-1082.
DOI: 10.3872/j.issn.1007-385X.2018.10.017
Abstract:
[摘要] 恶性黑色素瘤的发病率和病死率在逐年增长，引发广泛关注。目前恶性黑色素瘤的治疗方式主要为手术、化疗和靶向治疗，总体疗效极差。然而，PD-1 抗体治疗恶性黑色素瘤的成功，使广大研究者把希望聚焦于生物免疫治疗。肿瘤浸润淋巴细胞（tumor infiltrating lymphocyte，TIL）是从肿瘤组织分离出的淋巴细胞，经体外扩增后得到的能够杀伤肿瘤细胞的细胞群，具有高杀瘤活性和高靶向性特点。临床试验研究发现，TIL对恶性黑色素瘤治疗效果显著且稳定，但其临床疗效尚未完全阐明。本文对TIL免疫治疗的发展及其在恶性黑色素瘤治疗中的研究新进展作一综述，以期为恶性黑色素瘤的治疗提供新的策略。
[摘要] 恶性黑色素瘤的发病率和病死率在逐年增长，引发广泛关注。目前恶性黑色素瘤的治疗方式主要为手术、化疗和靶向治疗，总体疗效极差。然而，PD-1 抗体治疗恶性黑色素瘤的成功，使广大研究者把希望聚焦于生物免疫治疗。肿瘤浸润淋巴细胞（tumor infiltrating lymphocyte，TIL）是从肿瘤组织分离出的淋巴细胞，经体外扩增后得到的能够杀伤肿瘤细胞的细胞群，具有高杀瘤活性和高靶向性特点。临床试验研究发现，TIL对恶性黑色素瘤治疗效果显著且稳定，但其临床疗效尚未完全阐明。本文对TIL免疫治疗的发展及其在恶性黑色素瘤治疗中的研究新进展作一综述，以期为恶性黑色素瘤的治疗提供新的策略。
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.