LncRNA SNHG5 promotes cisplatin resistance in gastric cancer via inhibiting cell apoptosis.

Abstract

To elucidate the function of long non-coding RNA (lncRNA) SNHG5 in cisplatin-resistant gastric cancer (GC), and its potential mechanism. We detected the expressions of SNHG5, apoptosis-specific genes (Bax and Bcl-2) and drug resistance-specific genes (MDR1 and MRP1) in cisplatin-sensitive and cisplatin-resistant GC patients. The expression levels were also detected in cisplatin-resistant GC cell lines (BGC823/DDP, SGC7901/DDP) and GC cell lines (BGC823 and SGC7901). Through the liposome transfection, the regulatory effects of SNHG5 on proliferative potential and apoptosis were examined by cytotoxicity assay and flow cytometry assay, respectively. The protein levels of apoptosis-related genes and drug resistance-related genes influenced by SNHG5 were detected by Western blot. Compared with cisplatin-sensitive GC patients, SNHG5 expression was remarkably higher in cisplatin-resistant GC patients. Besides, higher SNHG5 expression was observed in BGC823/DDP and SGC7901/DDP cells relative to that of their parental cells. Proliferative rate (OD450) and IC50 decreased, but the apoptotic rate increased in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown. It is found that SNHG5 overexpression reduced cisplatin sensitivity in BGC823 and SGC7901 cells. Decreased cisplatin cytotoxicity, elevated IC50 and inhibited apoptotic rate were observed in GC cells overexpressing SNHG5. Moreover, the expression levels of Bax, MDR1 and MRP1 were upregulated, while Bcl-2 downregulated in BGC823 and SGC7901 cells overexpressing SNHG5. SNHG5 is highly expressed in cisplatin-resistant GC. SNHG5 promotes cisplatin resistance in GC by regulating apoptosis-related genes and drug resistance-related genes.