MicroRNA-217 acts as a tumor suppressor and correlates with the chemoresistance of cervical carcinoma to cisplatin.

Abstract

BackgroundMicroRNA-217 (miR-217) has been demonstrated to participate in the tumorigenesis and progression of various types of cancers. Nevertheless, the role of miR-217 in cervical carcinoma still remains not fully elucidated. This current work sought to investigate the role of miR-217 in the growth, migration, and invasion of cervical carcinoma and detect the role of miR-217 in the chemosensitivity of cervical carcinoma cell to cisplatin.Materials and methodsThe levels of miR-217 in 65 pairs of cervical carcinoma tissues and matched normal tissues were detected using quantitative real-time-PCR assay. The roles of miR-217 on the growth, apoptosis, migration, and invasion of cervical cancer SiHa and Ca-Ski cells were analyzed using Cell Counting Kit-8, flow cytometry, wound healing, and Transwell invasion assays, respectively. The target of miR-217 was identified using the online analysis tool TargetScan (http://www.targetscan.org/vert_72/) and was verified by luciferase reporter and immunoblotting assays. The xenograft tumor model was constructed to explore the impact of miR-217 on the growth of cervical carcinoma cell in vivo.ResultsThe level of miR-217 was remarkably lower in cervical carcinoma tissues than that in noncancerous tissues. Overregulation of miR-217 markedly suppressed the aggressiveness of cervical cancer cell and induced cell apoptosis through regulating V-Ki-Ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS). Finally, upregulation of miR-217 enhanced the chemosensitivity of both SiHa and Ca-Ski cervical cancer cells toward cisplatin.ConclusionAltogether, upregulation of miR-217 inhibits the aggressiveness phenotypes of cervical carcinoma cell via regulating KRAS gene and increases the sensitivity of cervical cancer cell to cisplatin.