Tao Pingping, Yang Binlie, Zhang Huiya, Sun Liyan, Wang Yungen, Zheng Weiping
Department of Obstetrics and Gynecology, Pudong New Area People's Hospital Affiliated to Shanghai Health University No. 490, Chuanhuan South Road, Pudong New District, Shanghai, China.
Department of Gynecology, Shaoxing People's Hospital, Shaoxing Hospital, Zhejiang University, School of Medicine No. 568 Zhongxing North Road, Yuecheng District, Shaoxing 201299, Zhejiang, China.
Int J Clin Exp Pathol. 2020 May 1;13(5):869-879. eCollection 2020.
Ovarian cancer is a common and fatal cancer in women. The long non-coding RNA (lncRNA) MEG3 was reported to affect the cellular processes of ovarian cancer, but the mechanisms remain unclear. Here, we aimed to explore the potential regulatory mechanism of MEG3 in ovarian cancer.
A reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was conducted to analyze the expression levels of MEG3 and miR-205-5p in tissues and cell lines. An MTT assay was utilized to determine the cell viability of ovarian cancer SKOV-3 and OVCAR-8 cells. A flow cytometry analysis was employed to disclose the ovarian cancer cell apoptosis. The migration and invasion of SKOV-3 and OVCAR-8 cells were examined using a Transwell assay. A bioinformatics analysis indicated miR-205-5p as a direct target of MEG3, and a luciferase reporter assay was conducted to validate the interaction between MEG3 and miR-205-5p.
MEG3 was significantly down-regulated, while miR-205-5p was up-regulated in ovarian cancer tissues and cell lines. The overexpression of MEG3 and the knockdown of miR-205-5p inhibited cell viability, migration and invasion but promoted the apoptosis rate in ovarian cancer cells. MiR-205-5p was identified as a downstream gene of MEG3 and is negatively regulated by MEG3. The introduction of miR-205-5p reversed the up-regulation of MEG3-mediated suppression effects on cell viability, migration and invasion and increased cell apoptosis in ovarian cancer cells.
The overexpression of lncRNA MEG3 inhibits cell proliferation and cell invasion and promotes apoptosis in ovarian cancer by sponging miR-205-5p.
卵巢癌是女性常见的致命性癌症。据报道,长链非编码RNA(lncRNA)MEG3会影响卵巢癌的细胞进程,但其机制尚不清楚。在此,我们旨在探究MEG3在卵巢癌中的潜在调控机制。
采用逆转录定量聚合酶链反应(RT-qPCR)分析组织和细胞系中MEG3和miR-205-5p的表达水平。利用MTT法测定卵巢癌SKOV-3和OVCAR-8细胞的细胞活力。采用流式细胞术分析揭示卵巢癌细胞凋亡情况。使用Transwell实验检测SKOV-3和OVCAR-8细胞的迁移和侵袭能力。生物信息学分析表明miR-205-5p是MEG3的直接靶点,并进行荧光素酶报告基因实验以验证MEG3与miR-205-5p之间的相互作用。
在卵巢癌组织和细胞系中,MEG3显著下调,而miR-205-5p上调。MEG3的过表达和miR-205-5p的敲低抑制了卵巢癌细胞的细胞活力、迁移和侵袭,但提高了细胞凋亡率。miR-205-5p被鉴定为MEG3的下游基因,并受到MEG3的负调控。miR-205-5p的导入逆转了MEG3介导的对细胞活力、迁移和侵袭的抑制作用的上调,并增加了卵巢癌细胞的凋亡。
lncRNA MEG3的过表达通过吸附miR-205-5p抑制卵巢癌细胞增殖和侵袭并促进其凋亡。