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Volume 25,Issue 1,2018 Table of Contents
2018, 25(1):1-8.
DOI: 10.3872/j.issn.1007-385X.2018.01.001
Abstract:
Nature killer(NK) cells possess an great potential on cancer immunotherapy without long term potential adverse events and unpredictable risks due to its biological characteristics, including MHC-independent recognition and rapid killing mechanisms to the target cell, using allogenic donor cells without GVHD, short circulation life span and low CRS risks. Although NK cells from PBMC shown an great tumor killing activities and less safety concerns than from other sources including stem cell and NK cell lines, but an efficient and safer protocols for NK cell expansion from PBMC still need to be improved. NK cell is considered as a great vector for chimera antigen receptors (CARs), however low efficiency of DNA transfection on primary NK cells is still the technically bottle neck for CAR-NK application. Clinical trails with NK cell therapy have shown encouraging efficacies on hematologic malignancy, but inconsistent on solid tumors because the NK cells that were produced from variety source cells and different protocols are differ from phenotype and function. In overall, significant progresses have made on NK cell immunotherapy in recent years, but challenges still ahead in term of manufacture and efficacy.
Nature killer(NK) cells possess an great potential on cancer immunotherapy without long term potential adverse events and unpredictable risks due to its biological characteristics, including MHC-independent recognition and rapid killing mechanisms to the target cell, using allogenic donor cells without GVHD, short circulation life span and low CRS risks. Although NK cells from PBMC shown an great tumor killing activities and less safety concerns than from other sources including stem cell and NK cell lines, but an efficient and safer protocols for NK cell expansion from PBMC still need to be improved. NK cell is considered as a great vector for chimera antigen receptors (CARs), however low efficiency of DNA transfection on primary NK cells is still the technically bottle neck for CAR-NK application. Clinical trails with NK cell therapy have shown encouraging efficacies on hematologic malignancy, but inconsistent on solid tumors because the NK cells that were produced from variety source cells and different protocols are differ from phenotype and function. In overall, significant progresses have made on NK cell immunotherapy in recent years, but challenges still ahead in term of manufacture and efficacy.
2018, 25(1):9-16.
DOI: 10.3872/j.issn.1007-385X.2018.01.002
Abstract:
The recent development of CRISPR-Cas systems (clustered regularly interspaced short palindromic repeat-clustered regularly interspaced short palindromic repeats associated system) as easily accessible and programmable tools for genome editing and regulation is spurring a revolution in biology.Experimental approaches based on this versatile technology have the potential to transform the field of cancer genetics. Here, we review current approaches for functional studies of urological cancer genes that are based on CRISPRCas systems, with emphasis on both advanced basic and translational urological research.
The recent development of CRISPR-Cas systems (clustered regularly interspaced short palindromic repeat-clustered regularly interspaced short palindromic repeats associated system) as easily accessible and programmable tools for genome editing and regulation is spurring a revolution in biology.Experimental approaches based on this versatile technology have the potential to transform the field of cancer genetics. Here, we review current approaches for functional studies of urological cancer genes that are based on CRISPRCas systems, with emphasis on both advanced basic and translational urological research.
2018, 25(1):17-22.
DOI: 10.3872/j.issn.1007-385X.2018.01.003
Abstract:
Bladder cancer is one of the most common malignant tumors of urinary system. It has been more and more difficult to diagnose and treat bladder cancer with old clinical models. Neo-biomarkers and actionable targets emerge with the incoming big data such as TCGA (the cancer genome atlas), MSK-IMPACT (Memorial Sloan-Kettering-integrated mutation profiling of actionable cancer targets),and HPA (human protein atlas) etc, providing more sufficient and reliable basis for the precise diagnosis, treatment and prognosis of bladder cancer. Precision medicine systems based on clinical data and omics information will be applied to the clinic more widely.More investment from government, lower cost and the constant development in new techniques represented with NGS (next generation sequencing) and liquid biopsy all make the precision medicine available from bench to bed, which will provide patients with more accurate and effective diagnosis and treatment. Here, we mainly summarize the development of precision medicine and its study and clinical application in bladder cancer.
Bladder cancer is one of the most common malignant tumors of urinary system. It has been more and more difficult to diagnose and treat bladder cancer with old clinical models. Neo-biomarkers and actionable targets emerge with the incoming big data such as TCGA (the cancer genome atlas), MSK-IMPACT (Memorial Sloan-Kettering-integrated mutation profiling of actionable cancer targets),and HPA (human protein atlas) etc, providing more sufficient and reliable basis for the precise diagnosis, treatment and prognosis of bladder cancer. Precision medicine systems based on clinical data and omics information will be applied to the clinic more widely.More investment from government, lower cost and the constant development in new techniques represented with NGS (next generation sequencing) and liquid biopsy all make the precision medicine available from bench to bed, which will provide patients with more accurate and effective diagnosis and treatment. Here, we mainly summarize the development of precision medicine and its study and clinical application in bladder cancer.
2018, 25(1):23-27.
DOI: 10.3872/j.issn.1007-385X.2018.01.004
Abstract:
Prostate cancer has become one of the most common malignant diseases in Chinese male. Hormonal therapy is an important and effective way to treat prostate cancer (especially advanced prostate cancer); however, some disputes merged from the clinical application are still to be solved. It seems crucial to unify the understanding and implement overall management to get satisfied effect in hormonal therapy of prostate cancer. According to guidelines and clinical trials in both domestic and overseas, we make a summary of series of problems that appeared in hormonal therapy of prostate cancer, such as treatment opportunity, treatment strategy, patients choose, prognosis and follow-up etc.
Prostate cancer has become one of the most common malignant diseases in Chinese male. Hormonal therapy is an important and effective way to treat prostate cancer (especially advanced prostate cancer); however, some disputes merged from the clinical application are still to be solved. It seems crucial to unify the understanding and implement overall management to get satisfied effect in hormonal therapy of prostate cancer. According to guidelines and clinical trials in both domestic and overseas, we make a summary of series of problems that appeared in hormonal therapy of prostate cancer, such as treatment opportunity, treatment strategy, patients choose, prognosis and follow-up etc.
2018, 25(1):28-34.
DOI: 10.3872/j.issn.1007-385X.2018.01.005
Abstract:
Due to the inherent resistance,renal cell carcinoma (RCC) is insensitive to radiotherapy and chemotherapy;thus, biotherapy is the only option for patients with metastatic renal cell carcinoma (mRCC). With the further understanding of RCC, small molecule targeted drug therapy has gradually replaced the previous cytokine therapy. In recent years, new immunotherapy has become the focus of research in the biotherapy of RCC. Small molecule targeted drug therapy and new immunotherapy have shown great advantages in the treatment, they can improve the survival time and quality of life for RCC patients; however,the low response rate, drug-esistance, side effects and other issues also appear. Thus, providing personalized treatment to bring greater benefits for RCC patients is the goal for clinical practitioners.
Due to the inherent resistance,renal cell carcinoma (RCC) is insensitive to radiotherapy and chemotherapy;thus, biotherapy is the only option for patients with metastatic renal cell carcinoma (mRCC). With the further understanding of RCC, small molecule targeted drug therapy has gradually replaced the previous cytokine therapy. In recent years, new immunotherapy has become the focus of research in the biotherapy of RCC. Small molecule targeted drug therapy and new immunotherapy have shown great advantages in the treatment, they can improve the survival time and quality of life for RCC patients; however,the low response rate, drug-esistance, side effects and other issues also appear. Thus, providing personalized treatment to bring greater benefits for RCC patients is the goal for clinical practitioners.
2018, 25(1):35-39.
DOI: 10.3872/j.issn.1007-385X.2018.01.006
Abstract:
Objective: To study the effects of synthetic small molecule double-stranded RNA-625（dsP21-625）on the activation of P21 gene in prostate cancer cells and its effect on cell proliferation. Methods: dsCtrl (control group) and dsP21-625（experimental group）were transfected into prostate cancer PC-3 and DU-145 cell lines. qPCR and Western blotting were used to detect the mRNA and protein expressions of P21, Cyclin E and cyclin dependent kinase 2（CDK2）in prostate cancer cells of each group after transfection. The cell cycle distribution, cell proliferation and clone formation were analyzed by flow cytometry, MTT assay and colony formation assay,respectively. Results: Compared with dsCtrl control group, P21 mRNA level was elevated in PC-3 cells and in DU-145 cells (all P<0.01) after transfection with dsP21-625; in the meanwhile, the expression of Cyclin E and CDK2 mRNA were down-regulated (P<0.01).The expression of P21 protein in PC-3 and DU-145 cells transfected with dsP21-625 was up-regulated (all P<0.01) while the expressions of Cyclin E and CDK2 proteins were down-regulated (all P<0.01); the proportion of cells in S phase and G2 / M phase decreased (all P<0.05), and the proportion of cells in G0/G1 phase increased (all P<0.01) after dsP21-625 transfection. The cell proliferation ability and colony formation were significantly decreased in dsP21-625 groups (all P<0.05). Conclusion: dsP21-625 can activate the expression of P21 mRNA and protein in prostate cancer cells, down-regulate the expression of Cyclin E and CDK2 protein, and significantly inhibit the proliferation of prostate cancer cells.
Objective: To study the effects of synthetic small molecule double-stranded RNA-625（dsP21-625）on the activation of P21 gene in prostate cancer cells and its effect on cell proliferation. Methods: dsCtrl (control group) and dsP21-625（experimental group）were transfected into prostate cancer PC-3 and DU-145 cell lines. qPCR and Western blotting were used to detect the mRNA and protein expressions of P21, Cyclin E and cyclin dependent kinase 2（CDK2）in prostate cancer cells of each group after transfection. The cell cycle distribution, cell proliferation and clone formation were analyzed by flow cytometry, MTT assay and colony formation assay,respectively. Results: Compared with dsCtrl control group, P21 mRNA level was elevated in PC-3 cells and in DU-145 cells (all P<0.01) after transfection with dsP21-625; in the meanwhile, the expression of Cyclin E and CDK2 mRNA were down-regulated (P<0.01).The expression of P21 protein in PC-3 and DU-145 cells transfected with dsP21-625 was up-regulated (all P<0.01) while the expressions of Cyclin E and CDK2 proteins were down-regulated (all P<0.01); the proportion of cells in S phase and G2 / M phase decreased (all P<0.05), and the proportion of cells in G0/G1 phase increased (all P<0.01) after dsP21-625 transfection. The cell proliferation ability and colony formation were significantly decreased in dsP21-625 groups (all P<0.05). Conclusion: dsP21-625 can activate the expression of P21 mRNA and protein in prostate cancer cells, down-regulate the expression of Cyclin E and CDK2 protein, and significantly inhibit the proliferation of prostate cancer cells.
2018, 25(1):40-44.
DOI: 10.3872/j.issn.1007-385X.2018.01.007
Abstract:
Objective: To investigate the expression of miR-1271-5p in renal cell carcinoma（RCC）tissues and cell lines and its effect on the proliferation and apoptosis of RCC A-498 cell line. Methods: Pathologically confirmed RCC tissues and para-cancerous tissues were collected. Real-time fluorescent quantitative PCR（qPCR）was used to analyze the expression of miR-1271-5p in collected RCC tissues and RCC cell lines (ACHN, A498, HK-2, 786-O, CaKi-1) as well as human embryonic kidney cell line HEK293. miR-1271-5p (experiment group) and miR-NC (control group) were transfected into A-498 cells, spectively. Bioinformatics predicts that DOCK1 is a possible target gene for miR-1271-5p. Double luciferase reporter gene vector of DOCK1 gene 3 'UTR (both wild and mutant type)were constructed and the luciferase activity was detected. The expression of DOCK1 mRNA was detected by qPCR. Western blotting was used to analyze the protein expressions of DOCK1, p-ERK, p-AKT, Bcl-2 and Bax in two groups of cells. MTS assay and colony formation assay were performed to detect cell viability and proliferation. Cell apoptosis was analyzed by flow cytometry. Results：Compared with para-cancerous tissue and human embryonic kidney cells, the expression of miR-1271-5p was significantly decreased in RCC tissues and cell lines (P<0.01). Double luciferase reporter gene system showed that DOCK1 is a target gene of miR-1271-5p (P<0.01). Compared with miR-NC transfected cells, the expression of DOCK1 mRNA in A-498 cells transfected with miR-1271-5p was significantly decreased (P<0.01); the protein expressions of DOCK1, p-ERK, p-AKT and Bcl-2 were significantly down-regulated（P<0.05）while the expression of Bax protein was significantly up-regulated (P<0.05); The viability and colony formation of A-498 cells was significantly decreased (all P<0.01), while apoptosis was ignificantly increased (P<0.01). Conclusion: miR-1271-5p was downregulated in RCC tissues and cell lines. miR-1271-5p significantly inhibited the proliferation and induced apoptosis of RCC A-489 cell by interfering with the expression of DOCK1 gene. This provides a theoretical basis for miR-1271-5p as a promise molecular target in RCC treatment.
Objective: To investigate the expression of miR-1271-5p in renal cell carcinoma（RCC）tissues and cell lines and its effect on the proliferation and apoptosis of RCC A-498 cell line. Methods: Pathologically confirmed RCC tissues and para-cancerous tissues were collected. Real-time fluorescent quantitative PCR（qPCR）was used to analyze the expression of miR-1271-5p in collected RCC tissues and RCC cell lines (ACHN, A498, HK-2, 786-O, CaKi-1) as well as human embryonic kidney cell line HEK293. miR-1271-5p (experiment group) and miR-NC (control group) were transfected into A-498 cells, spectively. Bioinformatics predicts that DOCK1 is a possible target gene for miR-1271-5p. Double luciferase reporter gene vector of DOCK1 gene 3 'UTR (both wild and mutant type)were constructed and the luciferase activity was detected. The expression of DOCK1 mRNA was detected by qPCR. Western blotting was used to analyze the protein expressions of DOCK1, p-ERK, p-AKT, Bcl-2 and Bax in two groups of cells. MTS assay and colony formation assay were performed to detect cell viability and proliferation. Cell apoptosis was analyzed by flow cytometry. Results：Compared with para-cancerous tissue and human embryonic kidney cells, the expression of miR-1271-5p was significantly decreased in RCC tissues and cell lines (P<0.01). Double luciferase reporter gene system showed that DOCK1 is a target gene of miR-1271-5p (P<0.01). Compared with miR-NC transfected cells, the expression of DOCK1 mRNA in A-498 cells transfected with miR-1271-5p was significantly decreased (P<0.01); the protein expressions of DOCK1, p-ERK, p-AKT and Bcl-2 were significantly down-regulated（P<0.05）while the expression of Bax protein was significantly up-regulated (P<0.05); The viability and colony formation of A-498 cells was significantly decreased (all P<0.01), while apoptosis was ignificantly increased (P<0.01). Conclusion: miR-1271-5p was downregulated in RCC tissues and cell lines. miR-1271-5p significantly inhibited the proliferation and induced apoptosis of RCC A-489 cell by interfering with the expression of DOCK1 gene. This provides a theoretical basis for miR-1271-5p as a promise molecular target in RCC treatment.
2018, 25(1):45-50.
DOI: 10.3872/j.issn.1007-385X.2018.01.008
Abstract:
Objective: To detect expression of miR-372-3p in the bladder cancer cell transfected with miR-372-3p mimics and to explore effect of miR-372-3p on proliferation, migration and invasion of the bladder cancer 5637 and T24 cell lines. Methods: Using lipofection,miR-372-3p mimics or miR-NC was transfected into the bladder cancer 5637 and T24 cells. Expressions of miR-372-3p mRNA and ATAD2 mRNA, expressions of ADAD2, E-cadherin and N-cadherin proteins, cell cycle distribution, viability of cell, cell proliferation ability, cell migration ability and cell invasion ability in the bladder cancer cells transfected with miR-372-3p mimics and miR-NC were respectively detected by qPCR, Western blotting assay, flow cytometry, MTT assay, colony forming test, scratch assay and Transwell assay. Results: Comparing with the bladder cancer cell transfected with miR-NC, expression of miR-372-3p mRNA significantly increased, expressions of ATAD2 mRNA and protein obviously decreased, expression of E-cadherin protein raised, expression of N-cadherin protein came down, cell cycle obviously arrested, abilities of cell viability and proliferation markedly reduced as well as cell numbers of migration and invasion reduced, in the bladder cancer cell transfected with miR-372-3p mimics. Conclusion: Low expression of miR-372-3p might be associated with occurrence and development of the bladder carcinoma. miR-372-3p could inhibit abilities of proliferation,migration and invasion of the bladder cancer cell through targeting control. It could be a novel target in biotherapy of the bladder carcinoma.
Objective: To detect expression of miR-372-3p in the bladder cancer cell transfected with miR-372-3p mimics and to explore effect of miR-372-3p on proliferation, migration and invasion of the bladder cancer 5637 and T24 cell lines. Methods: Using lipofection,miR-372-3p mimics or miR-NC was transfected into the bladder cancer 5637 and T24 cells. Expressions of miR-372-3p mRNA and ATAD2 mRNA, expressions of ADAD2, E-cadherin and N-cadherin proteins, cell cycle distribution, viability of cell, cell proliferation ability, cell migration ability and cell invasion ability in the bladder cancer cells transfected with miR-372-3p mimics and miR-NC were respectively detected by qPCR, Western blotting assay, flow cytometry, MTT assay, colony forming test, scratch assay and Transwell assay. Results: Comparing with the bladder cancer cell transfected with miR-NC, expression of miR-372-3p mRNA significantly increased, expressions of ATAD2 mRNA and protein obviously decreased, expression of E-cadherin protein raised, expression of N-cadherin protein came down, cell cycle obviously arrested, abilities of cell viability and proliferation markedly reduced as well as cell numbers of migration and invasion reduced, in the bladder cancer cell transfected with miR-372-3p mimics. Conclusion: Low expression of miR-372-3p might be associated with occurrence and development of the bladder carcinoma. miR-372-3p could inhibit abilities of proliferation,migration and invasion of the bladder cancer cell through targeting control. It could be a novel target in biotherapy of the bladder carcinoma.
9 Recombinant protein PTD-CHMP1A inhibits malignant biological behavior of renal cell carcinoma cells
2018, 25(1):51-55.
DOI: 10.3872/j.issn.1007-385X.2018.01.009
Abstract:
Objective: To study the influence of PTD-CHMP1A (protein transduction domain-chromatin modifying protein 1A) fusion proteins on proliferation, migration and invasion of renal cell carcinoma (RCC) cells in vitro and the growth of transplanted tumor in vivo.Methods: RCC A498 and 786-0 cells were treated with PTD-CHMP1A (1, 5, and 20 μg/ml), CHMP1A (5 μg/ml) and PBS respectively.The effect of PTD-CHMP1A on the proliferation of A498 cells was detected by MTT assay. The effect of PTD-CHMP1A on the migration of A498 cells was detected by scratch assay. The effect of PTD-CHMP1A on the invasion ability of A498 and 786-0 cells was detected by Transwell invasion assay. Finally, the transplanted tumor models were constructed by injecting 5×105 A498 cells into nude mice, and the effect of 20 μg PTD-CHMP1A on tumor growth was observed. Results: Compared with CHMP1A and PBS groups, PTDCHMP1A fusion proteins (1, 5, and 20 μg/ml) showed a significantly restrained effect on the proliferation of A498 tumor cells, which was in dose-dependent and time-dependent manners. 5 μg/ml of PTD-CHMP1A fusion proteins could effectively inhibit the migration of A498 cells (P<0.01 compared with CHMP1A group), and the invasion of A498 and 786-0 cells (compared with Chmp1A group, P<0.05), besides, PTD-CHMP1A inhibited the invasion of A498 cells in a dose-dependent manner. Furthermore, PTD-CHMP1A could also observably inhibit tumor growth in vivo. Conclusion: PTD-CHMP1A fusion proteins effectively inhibited the proliferation, migration and invasion of RCC cells and the growth of transplanted tumor.
Objective: To study the influence of PTD-CHMP1A (protein transduction domain-chromatin modifying protein 1A) fusion proteins on proliferation, migration and invasion of renal cell carcinoma (RCC) cells in vitro and the growth of transplanted tumor in vivo.Methods: RCC A498 and 786-0 cells were treated with PTD-CHMP1A (1, 5, and 20 μg/ml), CHMP1A (5 μg/ml) and PBS respectively.The effect of PTD-CHMP1A on the proliferation of A498 cells was detected by MTT assay. The effect of PTD-CHMP1A on the migration of A498 cells was detected by scratch assay. The effect of PTD-CHMP1A on the invasion ability of A498 and 786-0 cells was detected by Transwell invasion assay. Finally, the transplanted tumor models were constructed by injecting 5×105 A498 cells into nude mice, and the effect of 20 μg PTD-CHMP1A on tumor growth was observed. Results: Compared with CHMP1A and PBS groups, PTDCHMP1A fusion proteins (1, 5, and 20 μg/ml) showed a significantly restrained effect on the proliferation of A498 tumor cells, which was in dose-dependent and time-dependent manners. 5 μg/ml of PTD-CHMP1A fusion proteins could effectively inhibit the migration of A498 cells (P<0.01 compared with CHMP1A group), and the invasion of A498 and 786-0 cells (compared with Chmp1A group, P<0.05), besides, PTD-CHMP1A inhibited the invasion of A498 cells in a dose-dependent manner. Furthermore, PTD-CHMP1A could also observably inhibit tumor growth in vivo. Conclusion: PTD-CHMP1A fusion proteins effectively inhibited the proliferation, migration and invasion of RCC cells and the growth of transplanted tumor.
DING Xin
,
LYU Zhonglin
,
XU Ke
,
HOU Chunmei
,
XIAO He
,
WANG Renxi
,
HAN Gencheng
,
FENG Jiannan
,
LI Yan
,
SHEN Beifen
,
CHEN Guojiang
2018, 25(1):56-61.
DOI: 10.3872/j.issn.1007-385X.2018.01.010
Abstract:
Objective: To investigate the effect of granulocyte-macrophage colony stimulating factor（GM-CSF）on liver metastasis of colon cancer and the underlying mechanisms. Methods: GM-CSF gene and shRNA targeting GM-CSF were stably transfected into human colon cancer HCT116 and SW480 cell lines, respectively; the expression of GM-CSF was detected by ELISA. Liver metastasis model of colon cancer was established by injecting cancer cells into spleen. Some of the model mice were intraperitoneally injected with recombinant human GM-CSF every other day (3 μg，0.6 μg/mice). Four weeks after model establishment，liver gross and tumor metastasis were observed. The expression of N-cadherin and matrix metalloproteinase 2 (MMP2) was detected by Real-time fluorescent quantitative PCR while E-cadherin was detected by Western blotting. Results: According the expression of GM-CSF, HCT116 cells were grouped into low, median and high expression subgroups (GMlo, GMint, GMhiHCT116); Meanwhile, GMKDSW480 group (GM-CSFknockdown) was established. Liver gross and pathological results showed that injecting of GM-CSF-overexpressed HCT116 cells or exogenous GM-CSF remarkably increased the amounts of liver metastasis; In contrast, knockdown of GM-CSF showed the opposite effect.Furthermore，GM-CSF over-expression significantly up-regulated the levels of N-cadherin and MMP2 as well as down-regulated the levels of E-cadherin (P<0.05). Conclusion: GM-CSF can potently promote liver metastasis of colon cancer xenograft, which may be due to the down-regulation of E-cadherin and up-regulation of N-cadherin and MMP2.
Objective: To investigate the effect of granulocyte-macrophage colony stimulating factor（GM-CSF）on liver metastasis of colon cancer and the underlying mechanisms. Methods: GM-CSF gene and shRNA targeting GM-CSF were stably transfected into human colon cancer HCT116 and SW480 cell lines, respectively; the expression of GM-CSF was detected by ELISA. Liver metastasis model of colon cancer was established by injecting cancer cells into spleen. Some of the model mice were intraperitoneally injected with recombinant human GM-CSF every other day (3 μg，0.6 μg/mice). Four weeks after model establishment，liver gross and tumor metastasis were observed. The expression of N-cadherin and matrix metalloproteinase 2 (MMP2) was detected by Real-time fluorescent quantitative PCR while E-cadherin was detected by Western blotting. Results: According the expression of GM-CSF, HCT116 cells were grouped into low, median and high expression subgroups (GMlo, GMint, GMhiHCT116); Meanwhile, GMKDSW480 group (GM-CSFknockdown) was established. Liver gross and pathological results showed that injecting of GM-CSF-overexpressed HCT116 cells or exogenous GM-CSF remarkably increased the amounts of liver metastasis; In contrast, knockdown of GM-CSF showed the opposite effect.Furthermore，GM-CSF over-expression significantly up-regulated the levels of N-cadherin and MMP2 as well as down-regulated the levels of E-cadherin (P<0.05). Conclusion: GM-CSF can potently promote liver metastasis of colon cancer xenograft, which may be due to the down-regulation of E-cadherin and up-regulation of N-cadherin and MMP2.
11 MiR-129-5p influences the sensitivity of breast cancer MCF-7 cells to paclitaxel by regulating HMGB1
LU Lu
,
WANG Yunfeng
,
LYU Yidong
,
WANG Jie
,
WEI Yuanyu
,
CHANG Aimin
,
REN Jingjing
,
MA Dan
,
SHI Ying
2018, 25(1):62-67.
DOI: 10.3872/j.issn.1007-385X.2018.01.011
Abstract:
Objective: To investigate the effect of miR-129-5p on the sensitivity of breast cancer MCF-7 cells to paclitaxel (PTX) by regulating high mobility group box 1 (HMGB1). Methods: MCF-7 cells were transfected with miR-129-5p mimics or si-HMGB1 by liposomes transfection technology before stimulated with PTX, respectively. Then, the mRNA expressions of HMGB1 and miR-129-5p in MCF-7 cells were detected by Real-time fluorescence quantitative PCR. Assessment of the expression of HMGB1 protein in MCF-7 cells was performed using Western blotting, and the effect of PTX on the proliferation of MCF-7 cells was performed by CCK-8 assay.Finally, the effect of transfection on PTX-induced apoptosis of MCF-7 cells was detected by flow cytometry. Results: After being transfected with miR-129-5p mimics, the expression of miR-129-5p was significantly higher than that of the negative control group (P<0.01). Over-expression of miR-129-5p significantly enhanced the inhibition of MCF-7 cells proliferation by PTX (P< 0.05) and PTX-induced apoptosis (P<0.05), meanwhile it also significantly inhibited the xpression of HMGB1 mRNA and protein (all P<0.05). Transfection with si-HMGB1 significantly reduced the expression of HMGB1 mRNA and protein (all P<0.05) in MCF-7 cells. HMGB1 interference further promoted PTX-induced proliferation inhibition and apoptosis of MCF-7 cells (all P<0.05). Conclusion: miR-129-5p enhanced the sensitivity of MCF-7 cells to PTX by down-regulating HMGB1.
Objective: To investigate the effect of miR-129-5p on the sensitivity of breast cancer MCF-7 cells to paclitaxel (PTX) by regulating high mobility group box 1 (HMGB1). Methods: MCF-7 cells were transfected with miR-129-5p mimics or si-HMGB1 by liposomes transfection technology before stimulated with PTX, respectively. Then, the mRNA expressions of HMGB1 and miR-129-5p in MCF-7 cells were detected by Real-time fluorescence quantitative PCR. Assessment of the expression of HMGB1 protein in MCF-7 cells was performed using Western blotting, and the effect of PTX on the proliferation of MCF-7 cells was performed by CCK-8 assay.Finally, the effect of transfection on PTX-induced apoptosis of MCF-7 cells was detected by flow cytometry. Results: After being transfected with miR-129-5p mimics, the expression of miR-129-5p was significantly higher than that of the negative control group (P<0.01). Over-expression of miR-129-5p significantly enhanced the inhibition of MCF-7 cells proliferation by PTX (P< 0.05) and PTX-induced apoptosis (P<0.05), meanwhile it also significantly inhibited the xpression of HMGB1 mRNA and protein (all P<0.05). Transfection with si-HMGB1 significantly reduced the expression of HMGB1 mRNA and protein (all P<0.05) in MCF-7 cells. HMGB1 interference further promoted PTX-induced proliferation inhibition and apoptosis of MCF-7 cells (all P<0.05). Conclusion: miR-129-5p enhanced the sensitivity of MCF-7 cells to PTX by down-regulating HMGB1.
DENG Dawei
,
WU Bin
,
YAN Shu
,
LAN Chuan
,
ZHANG Guangnian
,
YI Pengsheng
,
ZENG Lijuan
,
LI Jianshui
2018, 25(1):68-72.
DOI: 10.3872/j.issn.1007-385X.2018.01.012
Abstract:
Objective: To explore the effect of forkhead box Q1（FOXQ1）gene silencing on in vitro angiopoiesis of pancreatic carcinoma cells, and to investigate its role in transforming growth factor-β1(TGF-β1) signaling pathway. Methods: FOXQ1-shRNA recombinant lentiviral vector and negative control lentiviral vector (NC-shRNA) were transfected into PANC-1 cells. Flow cytometry was used to detect the transfection efficiency. The gene silencing efficiency was measured by qPCR and Western blotting. FOXQ1-shRNA group,NC-shRNA group and blank group were set up. Human umbilical vein endothelial cells (HUVECs）were used for the in vitro angiopoiesis assay, which was observed under fluorescence microscopy. Meanwhile, qPCR and Western blotting were performed to examine mRNA and protein expressions of VEGF-A and MMP-2, respectively. After induction by TGF-β1 (final concentration of 5 ng/ml), the changes in angiopoiesis ability as well as the expression changes in FOXQ1，VEGF-A，MMP-2 in each group were detected. Results:The transfection efficiency of lentivirus was about 90%. Compared with NC-shRNA group, the angiopoiesis ability in FOXQ1-shRNA group was remarkably decreased（9.33±2.08 vs 28.67±2.52，P<0.05); Meanwhile, the expressions of VEGF-A and MMP-2 were all declined significantly (P<0.05). TGF-β1 improved the mRNA and protein expressions of FOXQ1，VEGF-A and MMP-2, and increased the in vitro angiopoiesis ability (P<0.05). Conclusion: FOXQ1 gene could mediate the in vitro angiopoiesis of PANC-1 cells; its mechanism may be related to the down-egulation of VEGF-A and MMP-2 and possibly be regulated by TGF-β1 pathway.
Objective: To explore the effect of forkhead box Q1（FOXQ1）gene silencing on in vitro angiopoiesis of pancreatic carcinoma cells, and to investigate its role in transforming growth factor-β1(TGF-β1) signaling pathway. Methods: FOXQ1-shRNA recombinant lentiviral vector and negative control lentiviral vector (NC-shRNA) were transfected into PANC-1 cells. Flow cytometry was used to detect the transfection efficiency. The gene silencing efficiency was measured by qPCR and Western blotting. FOXQ1-shRNA group,NC-shRNA group and blank group were set up. Human umbilical vein endothelial cells (HUVECs）were used for the in vitro angiopoiesis assay, which was observed under fluorescence microscopy. Meanwhile, qPCR and Western blotting were performed to examine mRNA and protein expressions of VEGF-A and MMP-2, respectively. After induction by TGF-β1 (final concentration of 5 ng/ml), the changes in angiopoiesis ability as well as the expression changes in FOXQ1，VEGF-A，MMP-2 in each group were detected. Results:The transfection efficiency of lentivirus was about 90%. Compared with NC-shRNA group, the angiopoiesis ability in FOXQ1-shRNA group was remarkably decreased（9.33±2.08 vs 28.67±2.52，P<0.05); Meanwhile, the expressions of VEGF-A and MMP-2 were all declined significantly (P<0.05). TGF-β1 improved the mRNA and protein expressions of FOXQ1，VEGF-A and MMP-2, and increased the in vitro angiopoiesis ability (P<0.05). Conclusion: FOXQ1 gene could mediate the in vitro angiopoiesis of PANC-1 cells; its mechanism may be related to the down-egulation of VEGF-A and MMP-2 and possibly be regulated by TGF-β1 pathway.
2018, 25(1):73-78.
DOI: 10.3872/j.issn.1007-385X.2018.01.013
Abstract:
Objective: To investigate the associations of MHC class I chain-related molecule A（MICA）gene polymorphism with susceptibility of breast cancer cells to NK cell-mediated cytotoxicity. Methods: MICA alleles of breast cancer cell lines（MCF-7, MDAMB-231, MDA-MB-435S and SK-BR-3）were analyzed by DNA sequencing. MICA protein expression in 293T cells transfected with MICA recombinant expression vectors (namely pMCFA5.1 ，pMCFA4 ，p231A5R ，p231A9 and p435A5P) was detected by Western blotting and Flow cytometry; the cytotoxicity of NK cells against the above 293T cells were measured by lactate dehydrogenase （LDH）assay and the release of perforin（PFN）and granzymes B（Gzm B）were measured by ELISPOT assay. Results: DNA sequencing result showed that MICA*008/A5.1 and MICA*001/A4 were expressed in MCF-7 cells, MICA*019/A5 and MICA*002/A9 were expressed in both MDA-MB-231 and SK-BR-3 cells while MICA*010/A5 was expressed in MDA-MB-435S cells. After the MICA recombinant expression vectors were transfected into 293T cells, the level of MICA were the lowest in pMCFA5.1 group (P<0.05), following after p435A5P group (P<0.05), and highly expressed in the pMCFA4, p231AR and p231A9 groups (P<0.05). NK cell-mediated cytotoxicity and the release of PFN and Gzm B: NK cell-mediated cytotoxicity were the lowest in p435A5P group (P<0.05), and the ability of inducing NK cells to release PFN and Gzm B was also the lowest in p435A5P group (P<0.05), but there were no statistical difference among the other transfected groups (P>0.05). Conclusion: MICA gene polymorphism is closely associated with susceptibility of breast cancer cells to NK cell-mediated cytotoxicity.
Objective: To investigate the associations of MHC class I chain-related molecule A（MICA）gene polymorphism with susceptibility of breast cancer cells to NK cell-mediated cytotoxicity. Methods: MICA alleles of breast cancer cell lines（MCF-7, MDAMB-231, MDA-MB-435S and SK-BR-3）were analyzed by DNA sequencing. MICA protein expression in 293T cells transfected with MICA recombinant expression vectors (namely pMCFA5.1 ，pMCFA4 ，p231A5R ，p231A9 and p435A5P) was detected by Western blotting and Flow cytometry; the cytotoxicity of NK cells against the above 293T cells were measured by lactate dehydrogenase （LDH）assay and the release of perforin（PFN）and granzymes B（Gzm B）were measured by ELISPOT assay. Results: DNA sequencing result showed that MICA*008/A5.1 and MICA*001/A4 were expressed in MCF-7 cells, MICA*019/A5 and MICA*002/A9 were expressed in both MDA-MB-231 and SK-BR-3 cells while MICA*010/A5 was expressed in MDA-MB-435S cells. After the MICA recombinant expression vectors were transfected into 293T cells, the level of MICA were the lowest in pMCFA5.1 group (P<0.05), following after p435A5P group (P<0.05), and highly expressed in the pMCFA4, p231AR and p231A9 groups (P<0.05). NK cell-mediated cytotoxicity and the release of PFN and Gzm B: NK cell-mediated cytotoxicity were the lowest in p435A5P group (P<0.05), and the ability of inducing NK cells to release PFN and Gzm B was also the lowest in p435A5P group (P<0.05), but there were no statistical difference among the other transfected groups (P>0.05). Conclusion: MICA gene polymorphism is closely associated with susceptibility of breast cancer cells to NK cell-mediated cytotoxicity.
2018, 25(1):79-84.
DOI: 10.3872/j.issn.1007-385X.2018.01.014
Abstract:
Objective: To investigate the effect of long-chain non-coding RNA metastasis-associated lung adenocarcinoma transcript 1（lncRNA MALAT1）on the malignant biological behavior of pancreatic cancer cells by regulating miR-204 expression and its possible mechanisms. Methods: Six pairs of pancreatic cancer tissues and corresponding para-cancerous tissues were sampled during surgery from October 2016 to December 2016 in Henan Provincial Hospital of Traditional Chinese Medicine. qPCR was used to detect the expression of lncRNA MALAT1 in pancreatic cancer tissues, adjacent normal tissues and different pancreatic cancer cells（BxPC-3，HS-7667，PANC-1，AsPC-1 and SW-1990). Double luciferase reporter gene assay was used to detect the interaction between MALAT1 and miR-204. Flow cytometry was used to determine the effect of MALAT1 on cell cycle and apoptosis of pancreatic cancer cells. The effects of MALAT1 and miR-204 on the migration and invasion of pancreatic cancer cells were examined by Wound-healing assay and Transwell invasion assay, respectively. The effect of MALAT1 on EMT-related proteins was detected by Western blotting. Results:Compared with para-cancer tissue, the expression of lncRNA MALAT1 in pancreatic cancer tissues was significantly increased (1.85±0.52 vs 0.34±0.12，P<0.05). The expression level of lncRNA MALAT1 in pancreatic cancer SW-1990 cell line was the highest (P<0.05). lncRNA MALAT1 could bind specifically to the 3 'UTR of miR- 204 to modulate the expression of miR- 204. Inhibition of MALAT1 expression could induce G2/M cell cycle arrest, and thus promote SW-1990 cell apoptosis; moreover, the ability of migration and invasion of SW-1990 cells was weakened and EMT-related proteins (N-cadherin, E-adherin and vimentin) were down-regulated after inhibiting the expression of MALAT1. However, over-expression of miR-204 could promote the migration and invasion of SW-1990 cells. Conclusion: lncRNA MALAT1 plays an important role in the development and progression of pancreatic cancer. It can regulate the malignant biological behavior of pancreatic cancer cells by targeting miR-204.
Objective: To investigate the effect of long-chain non-coding RNA metastasis-associated lung adenocarcinoma transcript 1（lncRNA MALAT1）on the malignant biological behavior of pancreatic cancer cells by regulating miR-204 expression and its possible mechanisms. Methods: Six pairs of pancreatic cancer tissues and corresponding para-cancerous tissues were sampled during surgery from October 2016 to December 2016 in Henan Provincial Hospital of Traditional Chinese Medicine. qPCR was used to detect the expression of lncRNA MALAT1 in pancreatic cancer tissues, adjacent normal tissues and different pancreatic cancer cells（BxPC-3，HS-7667，PANC-1，AsPC-1 and SW-1990). Double luciferase reporter gene assay was used to detect the interaction between MALAT1 and miR-204. Flow cytometry was used to determine the effect of MALAT1 on cell cycle and apoptosis of pancreatic cancer cells. The effects of MALAT1 and miR-204 on the migration and invasion of pancreatic cancer cells were examined by Wound-healing assay and Transwell invasion assay, respectively. The effect of MALAT1 on EMT-related proteins was detected by Western blotting. Results:Compared with para-cancer tissue, the expression of lncRNA MALAT1 in pancreatic cancer tissues was significantly increased (1.85±0.52 vs 0.34±0.12，P<0.05). The expression level of lncRNA MALAT1 in pancreatic cancer SW-1990 cell line was the highest (P<0.05). lncRNA MALAT1 could bind specifically to the 3 'UTR of miR- 204 to modulate the expression of miR- 204. Inhibition of MALAT1 expression could induce G2/M cell cycle arrest, and thus promote SW-1990 cell apoptosis; moreover, the ability of migration and invasion of SW-1990 cells was weakened and EMT-related proteins (N-cadherin, E-adherin and vimentin) were down-regulated after inhibiting the expression of MALAT1. However, over-expression of miR-204 could promote the migration and invasion of SW-1990 cells. Conclusion: lncRNA MALAT1 plays an important role in the development and progression of pancreatic cancer. It can regulate the malignant biological behavior of pancreatic cancer cells by targeting miR-204.
DENG Jiaqiu
,
FENG Dekui
,
LYU Shenghui
,
MA Guohui
,
ZOU Jiang
,
LAI Zhiheng
,
WANG Hong
,
CHEN Xiaoli
2018, 25(1):85-88.
DOI: 10.3872/j.issn.1007-385X.2018.01.015
Abstract:
Objective: To study the expressions of miR-21, miR-217, miR-29b and miR-92a-1 in the blood serum，feces and cancer tissues of colorectal cancer (CRC) patients and to explore their clinical significance. Methods: A total of 63 CRC patients treated in Hainan Provincial Hospital of Traditional Chinese Medicine from July 2016 to May 2017 were involved in this study. Based on metastasis or not, the patients were divided into non-metastasis group (n=35) and metastasis group (n=28). Meanwhile, another 30 health volunteers were included in the control group. Feces and blood samples were collected from all subjects and tumor tissues were harvested from CRC patients. Reverse transcription- polymerase chain reaction was employed to measure the expression level of miR-21, miR-217,miR-29b and miR-92a-1 in all samples. Results: Expression of serum miR-21, miR-217, miR-29b and miR-92a-1 in CRC patients was significantly higher than those in control subjects (all P<0.05) with the highest level in metastasis group (P<0.05). Expressions of miR-21, miR-217and miR-92a-1 in the feces of CRC patients were significantly higher than those of controls (all P<0.05); and the expression in non-metastasis group was significantly lower than that in metastasis group (P<0.05), but there was no obvious difference in expression levels of miR-21, miR-29b and miR-92a-1 between the non-metastasis group and the metastasis group (P>0.05). The expression levels of miR-21, miR-29b and miR-92a-1 in CRC tissues of non-metastasis group was significantly lower than that of metastasis group (all P<0.05) while the expression of miR-217 was remarkably higher than that of the metastasis group (P<0.05). Conclusion:miR-21, miR-292, miR-29b and miR-92a-1 were abnormally expressed in the blood serum, feces and tumor tissues of CRC patients,and the combined detection of multiple miRNAs is beneficial for evaluating the occurrence, diagnosis and prognosis of CRC.
Objective: To study the expressions of miR-21, miR-217, miR-29b and miR-92a-1 in the blood serum，feces and cancer tissues of colorectal cancer (CRC) patients and to explore their clinical significance. Methods: A total of 63 CRC patients treated in Hainan Provincial Hospital of Traditional Chinese Medicine from July 2016 to May 2017 were involved in this study. Based on metastasis or not, the patients were divided into non-metastasis group (n=35) and metastasis group (n=28). Meanwhile, another 30 health volunteers were included in the control group. Feces and blood samples were collected from all subjects and tumor tissues were harvested from CRC patients. Reverse transcription- polymerase chain reaction was employed to measure the expression level of miR-21, miR-217,miR-29b and miR-92a-1 in all samples. Results: Expression of serum miR-21, miR-217, miR-29b and miR-92a-1 in CRC patients was significantly higher than those in control subjects (all P<0.05) with the highest level in metastasis group (P<0.05). Expressions of miR-21, miR-217and miR-92a-1 in the feces of CRC patients were significantly higher than those of controls (all P<0.05); and the expression in non-metastasis group was significantly lower than that in metastasis group (P<0.05), but there was no obvious difference in expression levels of miR-21, miR-29b and miR-92a-1 between the non-metastasis group and the metastasis group (P>0.05). The expression levels of miR-21, miR-29b and miR-92a-1 in CRC tissues of non-metastasis group was significantly lower than that of metastasis group (all P<0.05) while the expression of miR-217 was remarkably higher than that of the metastasis group (P<0.05). Conclusion:miR-21, miR-292, miR-29b and miR-92a-1 were abnormally expressed in the blood serum, feces and tumor tissues of CRC patients,and the combined detection of multiple miRNAs is beneficial for evaluating the occurrence, diagnosis and prognosis of CRC.
WU Youjun
,
CAO Zhiyu
,
ZHANG Qingjun
,
LIU Ruijun
,
WANG Yue
,
LYU Gang
,
ZHANG Xinhui
,
SUN Yongsheng
,
YANG Bo
2018, 25(1):89-93.
DOI: 10.3872/j.issn.1007-385X.2018.01.016
Abstract:
Objective: To explore and identify the influence of dendritic cell-cytokine induced killer cell （DC-CIK）on the number of blood circulating tumor cell (CTC), therapeutic efficacy and prognosis of patients with liver metastasis after radical resection of colorectal cancer. Methods: We retrospectively analyzed the clinical data of patients developing liver metastasis after radical resection of colorectal cancer (CRC) and treated in PLA 309th Hospital between July, 2009 and December, 2015, among whom 62 patients were administered DC-CIK plus conventional treatment (DC-CIK group) and 70 received only conventional treatment (conventional group). In addition, peripheral venous blood of 21 patients in DC-CIK group and 24 patients in conventional group were examined to clarify CTC number via CellSearch R immunomagnetic technology. The therapeutic efficacy was compared between the two groups. Results: The CTC number of patients in DC-CIK group decreased significantly after treatment (1.0±1.1 vs 2.7±2.0, P<0.01), while that in conventional group did not alter obviously (P>0.05). The resection rate of liver metastasis, objective response rate to treatment, patients’progression-free survival and overall survival of DC-CIK group were all superior than those of conventional group (P<0.05 or P<0.01).Conclusion: DC-CIK can decrease the number of CTC in CRC patients with liver metastasis after radical operation and prolong their survival; it has reliable anti-tumor effect under the precondition of standard execution.
Objective: To explore and identify the influence of dendritic cell-cytokine induced killer cell （DC-CIK）on the number of blood circulating tumor cell (CTC), therapeutic efficacy and prognosis of patients with liver metastasis after radical resection of colorectal cancer. Methods: We retrospectively analyzed the clinical data of patients developing liver metastasis after radical resection of colorectal cancer (CRC) and treated in PLA 309th Hospital between July, 2009 and December, 2015, among whom 62 patients were administered DC-CIK plus conventional treatment (DC-CIK group) and 70 received only conventional treatment (conventional group). In addition, peripheral venous blood of 21 patients in DC-CIK group and 24 patients in conventional group were examined to clarify CTC number via CellSearch R immunomagnetic technology. The therapeutic efficacy was compared between the two groups. Results: The CTC number of patients in DC-CIK group decreased significantly after treatment (1.0±1.1 vs 2.7±2.0, P<0.01), while that in conventional group did not alter obviously (P>0.05). The resection rate of liver metastasis, objective response rate to treatment, patients’progression-free survival and overall survival of DC-CIK group were all superior than those of conventional group (P<0.05 or P<0.01).Conclusion: DC-CIK can decrease the number of CTC in CRC patients with liver metastasis after radical operation and prolong their survival; it has reliable anti-tumor effect under the precondition of standard execution.
2018, 25(1):94-97.
DOI: 10.3872/j.issn.1007-385X.2018.01.017
Abstract:
目的: 探讨miR-370 和EGFR在肺癌组织中的表达及其与患者临床病理特征的关系。方法: 收集45 例肺癌及对应的正常肺组织标本，采用qPCR检测miR-370 和EGFR mRNA的表达，用双荧光素酶检测系统检测共转染野生型及突变型EGFR 3’UTR质粒和miR-370 mimics 后的荧光强度。分析miR-370 和EGFR的相关性及其与肺癌患者临床病理特征的相关性。结果:miR-370 在肺癌组织中的中位(P25,P75)表达水平显著低于正常肺组织[0.153（0.119，3.068）vs 0.875（0.026，6.145），P<0.05]，EGFR在肺癌组织中的表达水平显著高于正常肺组织[2.974（1.728，2.975）vs 2.081（0.897，4.873），P<0.05]，两者水平呈负相关(r=–0.361，P<0.01)。双荧光素酶检测显示EGFR 3’UTR可与miR-370 结合。miR-370 表达与肺癌患者的年龄、性别、地域、肿瘤分期、肿瘤大小和淋巴结转移等无相关性(P<0.05)。结论: 在肺癌组织中miR-370 低表达、EGFR高表达，两者的表达水平呈负相关，miR-370 表达水平与患者肿瘤分期、病理类型等临床病理特征无相关性。
目的: 探讨miR-370 和EGFR在肺癌组织中的表达及其与患者临床病理特征的关系。方法: 收集45 例肺癌及对应的正常肺组织标本，采用qPCR检测miR-370 和EGFR mRNA的表达，用双荧光素酶检测系统检测共转染野生型及突变型EGFR 3’UTR质粒和miR-370 mimics 后的荧光强度。分析miR-370 和EGFR的相关性及其与肺癌患者临床病理特征的相关性。结果:miR-370 在肺癌组织中的中位(P25,P75)表达水平显著低于正常肺组织[0.153（0.119，3.068）vs 0.875（0.026，6.145），P<0.05]，EGFR在肺癌组织中的表达水平显著高于正常肺组织[2.974（1.728，2.975）vs 2.081（0.897，4.873），P<0.05]，两者水平呈负相关(r=–0.361，P<0.01)。双荧光素酶检测显示EGFR 3’UTR可与miR-370 结合。miR-370 表达与肺癌患者的年龄、性别、地域、肿瘤分期、肿瘤大小和淋巴结转移等无相关性(P<0.05)。结论: 在肺癌组织中miR-370 低表达、EGFR高表达，两者的表达水平呈负相关，miR-370 表达水平与患者肿瘤分期、病理类型等临床病理特征无相关性。
2018, 25(1):98-103.
DOI: 10.3872/j.issn.1007-385X.2018.01.018
Abstract:
乳腺癌是女性最常见的、发病率位居恶性肿瘤首位的肿瘤。自噬是一种高度保守的溶酶体依赖性分解代谢途径,参与细胞的生理和病理过程，是细胞维持自稳态的重要机制之一，并对肿瘤的生物学有着复杂且重要的作用。Beclin1 是第一个在哺乳动物中发现的与自噬相关的抑癌基因，其作为自噬体形成过程中的重要分子之一，是调控细胞自噬活性的关键靶点。近年来的研究发现，Beclin1 与乳腺癌的发生发展及预后密切相关。其不仅可以降低乳腺癌的发生概率，也能促进乳腺癌的进展。同时，Beclin1 也参与影响乳腺癌的辅助治疗效果，既可以影响化疗药物诱导的乳腺癌细胞的凋亡，也是乳腺癌内分泌治疗耐药的主要原因之一。Beclin1 与HER2 之间的相互作用也影响着靶向药物的疗效。因此本文就Beclin1 与乳腺癌的发生发展及其在治疗中的作用进行综述。
乳腺癌是女性最常见的、发病率位居恶性肿瘤首位的肿瘤。自噬是一种高度保守的溶酶体依赖性分解代谢途径,参与细胞的生理和病理过程，是细胞维持自稳态的重要机制之一，并对肿瘤的生物学有着复杂且重要的作用。Beclin1 是第一个在哺乳动物中发现的与自噬相关的抑癌基因，其作为自噬体形成过程中的重要分子之一，是调控细胞自噬活性的关键靶点。近年来的研究发现，Beclin1 与乳腺癌的发生发展及预后密切相关。其不仅可以降低乳腺癌的发生概率，也能促进乳腺癌的进展。同时，Beclin1 也参与影响乳腺癌的辅助治疗效果，既可以影响化疗药物诱导的乳腺癌细胞的凋亡，也是乳腺癌内分泌治疗耐药的主要原因之一。Beclin1 与HER2 之间的相互作用也影响着靶向药物的疗效。因此本文就Beclin1 与乳腺癌的发生发展及其在治疗中的作用进行综述。
2018, 25(1):104-108.
DOI: 10.3872/j.issn.1007-385X.2018.01.019
Abstract:
近年来随着肿瘤研究的深入，长链非编码RNA（long non-coding RNA，lncRNA）受到高度重视，在肿瘤的发生、发展、治疗和预后等方面发挥重要的作用。组织分化诱导非蛋白编码RNA（tissue differentiation inducing non-protein coding RNA，TINCR）在表皮细胞分化中具有重要作用，可促进表皮形成，TINCR缺如时则表现为表皮形成障碍。研究发现TINCR在结直肠癌、胃癌、鳞状细胞癌、膀胱癌、乳腺癌、肝细胞癌和黑色素瘤等表达异常，TINCR与多种分子相互作用而影响基因转录及转录后过程，可加速肿瘤发展，研究TINCR在肿瘤中的作用对肿瘤早期诊断及预后评估具有重要意义，TINCR可作为多种肿瘤的标志物及治疗的潜在靶标。
近年来随着肿瘤研究的深入，长链非编码RNA（long non-coding RNA，lncRNA）受到高度重视，在肿瘤的发生、发展、治疗和预后等方面发挥重要的作用。组织分化诱导非蛋白编码RNA（tissue differentiation inducing non-protein coding RNA，TINCR）在表皮细胞分化中具有重要作用，可促进表皮形成，TINCR缺如时则表现为表皮形成障碍。研究发现TINCR在结直肠癌、胃癌、鳞状细胞癌、膀胱癌、乳腺癌、肝细胞癌和黑色素瘤等表达异常，TINCR与多种分子相互作用而影响基因转录及转录后过程，可加速肿瘤发展，研究TINCR在肿瘤中的作用对肿瘤早期诊断及预后评估具有重要意义，TINCR可作为多种肿瘤的标志物及治疗的潜在靶标。
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Supported by:Beijing E-Tiller Technology Development Co., Ltd.