| 黄红丽,李 静,宋 玉.MiR-202靶向调节EGFR介导的PI3K/AKT信号通路在紫杉醇治疗卵巢癌中的机制研究[J].肿瘤学杂志,2020,26(9):803-807. |
| MiR-202靶向调节EGFR介导的PI3K/AKT信号通路在紫杉醇治疗卵巢癌中的机制研究 |
| Research on Mechanism of Targeted Adjustment of the MiR-202 for EGFR Mediated PI3K/AKT Signaling Pathway in the Treatment of Ovarian Cancer with Paclitaxel |
| 投稿时间：2019-11-20 |
| DOI：10.11735/j.issn.1671-170X.2020.09.B010 |
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| 中文关键词: EGFR PI3K/AKT信号通路 卵巢癌 miR-202 |
| 英文关键词:EGFR PI3K/AKT signaling pathway ovarian cancer miR-202 |
| 基金项目:湖北省自然科学基金（1606220100625） |
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| 中文摘要: |
| 摘 要：［目的］ 探讨miR-202靶向调节EGFR介导的PI3K/AKT信号通路在紫杉醇治疗卵巢癌中的作用机制。［方法］ 以人卵巢癌细胞株A2780细胞作为研究对象，分别转染miR-NC、miR-202 mimics及shEGFR。采用MTT和Transwell实验检测各组细胞增殖、迁移及侵袭能力。采用qRT-PCR检测细胞中miR-202和EGFR mRNA表达量。采用Western blot检测EGFR、p-PI3K、PI3K、p-AKT和AKT蛋白水平。［结果］ qRT-PCR结果显示，与正常人卵巢上皮细胞HOSEpiC相比，miR-202在卵巢癌细胞A2780/WT 及A2780/PTX中明显低表达（P<0.05）；EGFR mRNA水平显著性上调（P<0.05）。转染miR-202 mimics后，卵巢癌细胞中miR-202相对表达量显著性高于miR-NC组和shEGFR组（P<0.05）；而miR-202 mimics组和shEGFR组EGFR mRNA含量显著性低于miR-NC组（P<0.05）。过表达miR-202及转染shEGFR后，miR-202 mimics组和shEGFR组细胞增殖能力较miR-NC组均显著性降低（P<0.05）；迁移细胞和侵袭数目也随之减少（P<0.05）；且对紫杉醇的半数抑制浓度IC50降低（P<0.05）。免疫印迹测定结果显示，miR-202 mimics组和shEGFR组中EGFR蛋白、p-PI3K/PI3K及p-AKT/AKT磷酸化水平较miR-NC组明显下调（P<0.05）。［结论］ miR-202能靶向调节EGFR表达，并且影响卵巢癌细胞的增殖、迁移及侵袭过程，其作用机制是通过抑制EGFR下游PI3K/AKT信号通路从而发挥抑癌作用，为临床治疗提供了新方向。 |
| 英文摘要: |
| Abstract：［Objective］ To explore the mechanism of targeted adjustment of miR-202 for EGFR mediated PI3K/AKT signaling pathway in the treatment of ovarian cancer with paclitaxel. ［Methods］ The human ovarian cancer cell lines -A2780 cells were selected as the research objects，and transfected with miR-NC，miR-202 mimics and shEGFR. MTT and Transwell experiments were used to determine the cell proliferation，migration and invasion ability in different groups. qRT-PCR was employed to detect the miR-202 level and EGFR mRNA expression. Meanwhile，Western blot was used to test EGFR，p-PI3K，PI3K，p-AKT and AKT protein levels. ［Results］ qRT-PCR results showed that miR-202 levels in A2780/WT and A2780/PTX clearly decreased compared with normal ovarian epithelial cells HOSEpiC(P<0.05)，and EGFR mRNA levels increased significantly(P<0.05). After transfecting with miR-202 mimics，miR-202 expression in ovarian cancer cells was significantly higher than that in miR-NC group and shEGFR group(P<0.05). However，EGFR mRNA expression in miR-202 mimics and shEGFR groups were significantly higher than that in miR-NC group(P<0.05). Due to the overexpression of miR-202 and transfection shEGFR，the cell proliferation ability of miR-202 mimics and shEGFR groups cell were significantly lower than that in miR-NC group(P<0.05). Moreover，the IC50 of paclitaxel obviously decreased(P<0.05). There were less migration and invasion cells(P<0.05). Western blot results showed that EGFR protein，p-PI3K/PI3K and p-AKT/AKT phosphorylation levels in miR-202 mimics and shEGFR groups were significantly lower than that in miR-NC group(P<0.05). ［Conclusion］ miR-202 target adjusts the expression of EGFR to affect cell proliferation，migration and attack process of ovarian cancer，which functions mainly via inhibiting EGFR downstream of PI3K/AKT signaling pathways and thus plays a role in tumor suppressor，which provides a new direction for clinical treatment. |
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