LncRNA BANCR Attenuates the Killing Capacity of Cisplatin on Gastric Cancer Cell through the ERK1/2 Pathway

Background: Chemotherapy-based comprehensive treatment is the most important therapeutic method for patients with advanced gastric cancer, but chemoresistance often causes treatment failure. Long non-coding RNA (LncRNA) BRAF-activated non-coding RNA (BANCR) has been shown to participate in many biological behaviors of multiple cancers. However, the biological roles of LncRNA BANCR in chemoresistance of gastric cancer remain unclear. Here, we aimed to evaluate the functions of LncRNA BANCR in the therapy of gastric cancer. Methods In this study, LncRNA BANCR expression was detected in GC patient samples and cell lines by quantity polymerase chain reaction (qPCR). Cell proliferation and viability in cisplatin treated cells were measured using clonogenic survival assay and cell counting kit-8. The levels of ERK1/2 pathway molecules were tested with western blot. Ly3214996, an inhibitor of ERK signal pathway, administration was used to assess the effects of BANCR overexpression on GC cell cisplatin-treated resistance. Moreover, the role of BANCR in cisplatin resistance of GC was certified in xenograft mouse models in vivo . Results our study showed that LncRNA BANCR expression was also significantly increased in GC tissues compared with adjacent normal tissues. Furthermore, we found that BANCR overexpression promoted, while BANCR inhibited, GC cell resistance to cisplatin in vitro . Ly3214996 treatment abolished the BANCR overexpression-mediated GC cell cisplatin resistance via regulating the phosphorylation of ERK protein. Knock-down of BANCR delayed significantly tumor growth in xenograft mouse models. Conclusion BANCR promoted cisplatin resistance of GC cells by activating ERK1/2 pathway. Inhibition of BANCR was markedly suppressed the growth of gastric cancer cells in vitro as well as in vivo . This result provided a new strategy for gastric cancer via targeting BANCR