RESUMO
Opa-interacting protein 5 antisense transcript 1 (OIP5-AS1) is one kind of cytoplasmic long non-coding RNA (lncRNA), which has been demonstrated to play a critical function in multiple cancers. However, the detailed mechanism of OIP5-AS1 in the regulation of cervical cancer progression is still obscure. Here, we demonstrated that lncRNA OIP5-AS1 was upregulated in cervical cancer and was correlated with poor prognosis by bioinformatics studies. OIP5-AS1 depletion inhibited cell proliferation and promoted cell apoptosis in cervical cancer cells. Furthermore, we clarified that ROCK1 was the downstream effector of OIP5-AS1 and OIP5-AS1 acted as a molecular sponge of miR-143-3p. Finally, we verified that OIP5-AS1 exerted its function in the regulation of cervical cancer progression via interacting with miR-143-3p to regulate ROCK1 expression. Our study revealed novel mechanisms about how lncRNA OIP5-AS1 executed its function in cervical cancer and thus provided potential therapeutic targets for the disease.
Assuntos
Humanos , Feminino , Neoplasias do Colo do Útero/patologia , Apoptose/fisiologia , MicroRNAs/metabolismo , Proliferação de Células/fisiologia , Quinases Associadas a rho/metabolismo , RNA Longo não Codificante/metabolismo , Regulação Neoplásica da Expressão Gênica , Regulação para Cima , Neoplasias do Colo do Útero/metabolismo , Western Blotting , Apoptose/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , MicroRNAs/genética , Linhagem Celular Tumoral , Proliferação de Células/genética , Quinases Associadas a rho/genética , RNA Longo não Codificante/genéticaRESUMO
@#[Abstract] Objective: To investigate the molecular mechanism of miR-143-3p regulating the proliferation, migration and invasion of colon cancer RKO cells via targeting enhancer of zeste homolog 2 (EZH2). Methods: A total of 40 pairs of colon cancer tissues and corresponding para-cancerous tissues resected in the First Affiliated Hospital of Kunming Medical University from March 2015 to July 2017 were collected for this study. In addition, colon cancer cell lines (COLO320, RKO and CL-11) and normal intestinal mucosa NCM460 cells were also collected. qPCR was applied to detect the expression level of miR-143-3p in colon cancer tissues and cell lines. miR-143-3p mimics, miR-143-3p inhibitor, EZH2 siRNA and negative control plasmids were transfected into RKO cells, respectively. The effect of miR-143-3p/EZH2 axis on the proliferation, migration and invasion of RKO cells were detected by CCK-8 and Transwell assay, respectively. Western blotting was used to detect the expression level of EZH2 protein in RKO cells. The targeting relationship between miR-143-3p and EZH2 was verified by Dual luciferase reporter gene assay. Results: The expression level of miR-143-3p was downregulated in colon cancer tissues and cell lines (all P<0.01). Overexpression of miR-143-3p significantly inhibited the proliferation, migration and invasion of RKO cells (all P<0.01). Dual luciferase reporter gene assay confirmed that EZH2 was a target gene of miR-143-3p. Simultaneous knockdown of miR-143-3p and EZH2 attenuated the inhibition of EZH2 knockdown on the proliferation, migration and invasion of RKO cells. Conclusion: miR-143-3p suppresses the proliferation, migration and invasion of colon cancer cells via targetedly down-regulating EZH2.