Knockdown of long non‑coding RNA LINC00152 increases cisplatin sensitivity in ovarian cancer cells
Affiliations: Department of Obstetrics and Gynecology, Beijing Shijitan Hospital of Capital Medical University, Beijing 100038, P.R. China
- Published online on: September 30, 2019 https://doi.org/10.3892/etm.2019.8066
Copyright: © Zou
et al. This is an open access article distributed under the
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Drug resistance severely limits the effectiveness of chemotherapeutic treatment in ovarian cancer. The present study aimed to investigate the role of long non‑coding RNA LINC00152 (LINC00152) in the cisplatin resistance of ovarian cancer. The expression level of LINC00152 was significantly increased in the ovarian cancer CoC1 and CoC1/DDP cell lines compared with the normal ovarian IOSE‑80 cell line. To further investigate the function of LINC00152, small interfering RNAs (siRNAs) targeting LINC00152 were transfected into COC1 and COC1/DDP cells, which were subsequently treated with varying concentrations of cisplatin. The results revealed that LINC00152 silencing increased the apoptotic rates and enhanced the chemosensitivity of CoC1 and CoC1/DDP cells to cisplatin. Furthermore, downregulation of LINC00152 significantly decreased Bcl‑2, and increased Bax and cleaved caspase‑3 expression levels. Additionally, LINC00152 silencing decreased the expression of multidrug resistance‑associated gene 1 (MDR1), multidrug resistance‑associated protein 1 (MRP1) and glutathione S‑transferase π (GSTπ). Collectively, the data demonstrated that LINC00152 knockdown increased the chemosensitivity of epithelial ovarian cancer cells to cisplatin by increasing apoptosis and decreasing the expression levels of MDR1, MRP1 and GSTπ.