MicroRNA‑654‑3p enhances cisplatin sensitivity by targeting QPRT and inhibiting the PI3K/AKT signaling pathway in ovarian cancer cells
- Yi‑Chao Niu
- Jing Tong
- Xiao‑Fei Shi
- Ting Zhang
Affiliations: Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, P.R. China, Department of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200126, P.R. China
- Published online on: June 11, 2020 https://doi.org/10.3892/etm.2020.8878
Copyright: © Niu
et al. This is an open access article distributed under the
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Dysregulation of microRNAs serves a crucial role in the chemosensitivity to cisplatin (DDP) in ovarian cancer (OVC). The abnormal expression of microRNA (miR)‑654‑3p has been reported in several types of human cancer. However, the association between miR‑654‑3p and cisplatin resistance in human OVC remains unclear. The present study aimed to investigate the role and mechanism of miR‑654‑3p in DDP resistance in OVC. The results demonstrated that miR‑654‑3p was significantly downregulated in ovarian cancer tissues and cells, as well as DDP‑resistant IGROV‑1/DDP cells, compared with adjacent non‑tumoral tissue and IOSE386 cells. Overexpression of miR‑654‑3p significantly suppressed the proliferation and migration of ovarian cancer cells and increased the sensitivity of IGROV‑1/DDP cells to DDP. Luciferase reporter assay demonstrated that quinolinate phosphoribosyl transferase (QPRT) was a target of miR‑654‑3p; overexpression of miR‑654‑3p inhibited QPRT expression by binding to the 3'‑untranslated region of QPRT. In addition, inhibition of miR‑654‑3p reversed the suppressive effects of QPRT‑targeting short interfering RNA on the proliferation and chemoresistance of ovarian cancer cells. Therefore, the results of the present study revealed a previously unrecognized regulatory mechanism that miR‑654‑3p enhances DDP sensitivity of OVC cells by downregulating QPRT expression; in addition, the present study highlighted the therapeutic implications of miR‑654‑3p upregulation in OVC.