Jia Guo, Hua Pan
Department of Obstetrics, Lanzhou Maternity and Child Health Care Hospital, Lanzhou, Gansu, China (mainland)
Med Sci Monit 2019; 25:9844-9854
Ovarian cancer (OC) is the most frequent aggressive cancer among women worldwide, and chemoresistance is the major challenge in the clinical treatment of OC. Recently, there is evidence that long noncoding RNAs (lncRNAs) are closely related to the regulation of cisplatin (CDDP) resistance in OC cells. However, whether LINC01125, a novel lncRNA, can improve the sensitivity of OC to cisplatin remains unknown.
MATERIAL AND METHODS: In this study, we analyzed aberrantly expressed lncRNAs in miR-200a-overexpressing OC samples by using GSE122123. LINC01125 and miR-1972 expressions were measured by qRT-PCR. The effect of LINC01125 overexpression on cell proliferation was determined by CCK-8 and colony formation assays. The sensitivity of OC cells to cisplatin was determined by CCK-8 assays. The interaction between LINC01125 and miR-1972 was verified through dual-luciferase reporter and RNA immunoprecipitation (RIP) assays, and bioinformatics analysis was performed to predict the target genes of miR-1972.
RESULTS: Our results indicated that LINC01125 expression was significantly downregulated in CDDP-resistant OC tissues and cell lines. Overexpression of LINC01125 inhibited OC cell proliferation and enhanced the cytotoxicity of CDDP in OC cells. Additionally, LINC01125 participated in the apoptosis pathway by directly binding to miR-1972 in OC cells.
CONCLUSIONS: Therefore, we suggest that LINC01125 might act as a tumor suppressor in OC and enhances the cisplatin sensitivity of OC cells by binding to miR-1972.
Keywords: Cisplatin, Ovarian Neoplasms, RNA, Long Noncoding