Open AccessKnockdown of long non‑coding RNA LINC00152 increases cisplatin sensitivity in ovarian cancer cells
Author(s) -
Hanxue Zou,
Hongxia Li
Publication year - 2019
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2019.8066
Subject(s) - gene knockdown , cisplatin , small interfering rna , ovarian cancer , gene silencing , biology , cancer research , apoptosis , transfection , cancer , cell culture , biochemistry , chemotherapy , gene , genetics
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.