[摘要] 目的：探讨miR-141-3p 通过靶向PTEN并调控PI3K/Akt 通路对卵巢癌细胞增殖、侵袭和凋亡的影响。方法：收集2014 年4 月至2017 年10 月河南省人民医院妇产科收治的资料完整的28 例卵巢癌患者肿瘤组织和相应的癌旁组织，采用qPCR检测卵巢癌组织和细胞系中miR-141-3p 的表达水平，双荧光素酶报告基因实验验证miR-141-3p 和PTEN的靶向关系；过表达或敲降miR-141 及PTEN基因后，采用CCK-8、Transwell 和Annexin V-FITC/PI 双染流式术检测卵巢癌A2780 细胞增殖、侵袭和凋亡水平，WB实验进一步检测miR-141-3p 对PTEN-PI3K/Akt 信号通路的调控作用。结果：miR-141-3p 在卵巢癌组织和细胞系中高表达（P<0.05 或P<0.01）。双荧光素酶报告基因证实miR-141-3p 靶向作用于PTEN并下调其表达水平（P<0.01）。与对照组相比，敲降miR-141-3p 后A2780 细胞的增殖受到显著抑制（48 h 时，0.36±0.04 vs 0.82±0.06，P<0.05）、侵袭能力明显降低[穿膜细胞数（45.14±7.88）vs（215.32±16.04）个，P<0.01]、细胞凋亡率显著升高[ （9.29±0.65）% vs（1.85±0.26）%，P<0.01]。过表达PTEN显著抑制了A2780 细胞中p-Akt 的表达（均P<0.01）、抑制细胞增殖和侵袭能力（均P<0.01）而明显促进细胞凋亡（均P<0.01），在过表达PTEN的同时过表达miR-141-3p 或添加IGF-1 后可逆转上述的变化。结论：miR-141-3p 能够促进A2780 细胞增殖、侵袭和诱导凋亡，其机制可能与靶向调控PTEN并激活PI3K/Akt通路有关。

[Abstract] Objective: To explore the effect of miR-141-3p on the proliferation, invasion and apoptosis of ovarian cancer cells via targeting PTEN and regulating PI3K/Akt pathway. Methods: Collecting twenty-eight cases pairs of ovarian cancerovarian cancer patients with tumor tissues and adjacent tissues were collected from patients, who from April 2014 to October 2017 were treated in the Department of Obstetrics and Gynecology. qPCR was applied to detect the expression of miR-141-3p in ovarian cancer tissues and cell lines.The relationship between miR-141-3p and PTEN was verified by dual-luciferase reporter gene assay. After over-expression or knockdown of miR-141 and PTEN genes, the cell viability, invasion and apoptosis of ovarian cancer A2780 cells were examined by CCK-8 assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Furthermore, the effect of miR-141-3p on PTEN-PI3K/Akt signaling pathway was measured by WB. Results: miR-141-3p is was highly expressed in ovarian cancer tissues and cell lines (P<0.05 or P<0.01). The dual luciferase reporter gene assay confirmed that miR-141-3p targets PTEN was a target of miR-141-3p and downregulates its expression level was down-regulated (P<0.01). Compared with the control group, after knockdown of miR-141-3p, the proliferation of A2780 cells was significantly inhibited after knockdown of miR-141-3p (at 48 h, 0.36±0.04 vs 0.82±0.06, P<0.05), and the invasive ability of A2780 cells was significantly reduced (number of transmembrane cells: 215.32±16.04 vs 45.14±7.88, P<0.01), while the apoptotic rate was significantly increased ([1.85±0.26]% vs [9.29±0.65]%, P<0.01). Over-expression of PTEN significantly inhibited the expression of p-Akt and cell proliferation and invasion in A2780 cells (all P<0.01), inhibited cell pro-liferation and invasion (all P<0.01) and significantly promoted apoptosis (all P<0.01). However, simultaneous over-expression of miR-141-3p or addition of IGF-1 wile over-expressing PTEN can offset the above effects. Conclusion: miR-141-3p facilitates the proliferation,invasion and decreases apoptosis of A2780 cells. The mechanism may be related to targeted regulation of PTEN and activation of PI3K/Akt pathway.