张猛, 张全, 谭雨莎. miR-497 靶向Bcl-2 调控肝癌细胞增殖及凋亡的研究[J]. 中国肿瘤临床, 2016, 43(16): 697-701. DOI: 10.3969/j.issn.1000-8179.2016.16.381
引用本文: 张猛, 张全, 谭雨莎. miR-497 靶向Bcl-2 调控肝癌细胞增殖及凋亡的研究[J]. 中国肿瘤临床, 2016, 43(16): 697-701. DOI: 10.3969/j.issn.1000-8179.2016.16.381
shu
Meng ZHANG, Quan ZHANG, Yusha TAN. miR-497 regulates cell proliferation and apoptosis by targeting Bcl-2 in liver cancer cells[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2016, 43(16): 697-701. DOI: 10.3969/j.issn.1000-8179.2016.16.381
Citation: Meng ZHANG, Quan ZHANG, Yusha TAN. miR-497 regulates cell proliferation and apoptosis by targeting Bcl-2 in liver cancer cells[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2016, 43(16): 697-701. DOI: 10.3969/j.issn.1000-8179.2016.16.381
shu

miR-497 靶向Bcl-2 调控肝癌细胞增殖及凋亡的研究

miR-497 regulates cell proliferation and apoptosis by targeting Bcl-2 in liver cancer cells

    摘要
  • 摘要: 目的：探讨miR-497 靶向Bcl- 2 对肝癌细胞增殖、凋亡的调控作用。方法：选取肝癌组织及相应远癌正常组织，分别采用逆转录PCR（reverse transcription PCR，RT-PCR）、Westernblot检测组织中miR-497 及Bcl- 2 蛋白表达；选取肝癌细胞系HepG2，分别转染miR-497 mimics 及对照寡核苷酸，采用RT-PCR、Westernblot检测组织中miR-497 及Bcl- 2 蛋白表达，采用MTT 法检测各组细胞增殖活性，采用流式细胞仪检测各组细胞凋亡，采用双荧光素酶报告基因检测细胞荧光酶活性。结果：1）与远癌正常组织相比，肝癌组织中miR-497 表达明显降低（P < 0.05），Bcl- 2 蛋白表达明显增高（P < 0.05）；2）与转染对照寡核苷酸相比，转染miR-497可使HepG2 中miR-497 表达增高（P < 0.05），Bcl- 2 蛋白表达降低（P < 0.05）；3）与转染对照寡核苷酸相比，共转染miR-497 与Bcl-2-WT可使HepG2 荧光素酶活性降低（P < 0.05）；4）转染miR-497 后，HepG2 增殖活性较转染对照寡核苷酸明显降低（P < 0.05），而转染miR-497 +Bcl-2 后，HepG2 增殖活性较单纯转染miR-497 明显提高（P < 0.05）；5）转染miR-497 后，HepG2 总凋亡比例较转染对照寡核苷酸明显增高（P < 0.05）；而转染miR-497 +Bcl-2 后，HepG2 总凋亡比例较单纯转染miR-497 明显降低（P < 0.05）。 结论：miR-497 可通过靶向Bcl- 2 抑制肝癌细胞增殖同时促进细胞凋亡。

     

    Abstract: Objective:To evaluate the effect of miR- 497 on regulating cell proliferation and apoptosis by targeting Bcl-2 in liver cancer cells. Methods: We tested liver cancer tissue and para-carcinoma tissue and used RT-PCR or Western blot to detect the expression of miR-497and Bcl-2 protein. We also tested the liver cancer cell HepG2 transfected with miR- 497 mimics and mimic control. The expressions of miR-497and Bcl-2 protein were detected by RT-PCR or Western blot. Cell proliferation activity was detected by the MTT method, cell apoptosis was detected by flow cytometry, and cell luciferase activity was detected by the dual-luciferase reporter gene experiment.Results:1) Compared with para-carcinoma tissue, the miR-497 expression of liver cancer tissue significantly decreased (P<0. 05), whereas the Bcl- 2 protein expression of liver cancer tissue significantly increased ( P<0.05 ). 2) Compared with transfection mimic control, transfection miR- 497 mimics could increase the miR-497 expression of liver cancer cell HepG 2 (P<0.05 ) and decrease the Bcl- 2 protein expression of liver cancer cell HepG 2(P<0.05 ). 3) Compared with transfection mimic control, co-transfection with miR- 497 mimics and Bcl-2-WT could significantly decrease the luciferase activity of liver cancer cell HepG 2 (P<0.05). 4) Compared with transfection mimic control, the proliferative activity of liver cancer cell HepG 2 significantly decreased after transfection with miR- 497 mimics (P<0. 05). Compared with transfection miR- 497 mimics, the proliferative activity of liver cancer cell HepG 2 significantly increased after transfection with miR- 497 mimics+Bcl- 2 (P<0.05). 5) Compared with transfection mimic control, the total apoptosis rate of liver cancer cell HepG2 significantly increased after transfection with miR-497 mimics (P<0.05). Compared with transfection miR-497 mimics, the total apoptosis rate of liver cancer cell HepG 2 significantly decreased after transfection with miR- 497 mimics+Bcl-2 (P<0.05 ). Conclusion: In liver cancer cells, miR- 497 could target Bcl-2 to inhibit cell proliferation and enhance cell apoptosis.

     

    • HTML全文
    • 参考文献(0)
    • 相关文章
    • 施引文献
  • 资源附件(0)

/

返回文章
返回