LncRNA Enhances Cisplatin Resistance by Regulating -mediated Apoptosis via in Human Gastric Cancer.

BACKGROUND

Chemoresistance contributes to treatment failure of gastric cancer (GC) patients but the molecular mechanism of chemoresistance in GC is still unclear. Long-chain noncoding RNA (lncRNA) urothelial cancer associated 1 () is associated with resistance to chemotherapy drugs.

METHODS

We detected the expression of in 53 pairs of GC tumor tissue and adjacent normal tissue, human normal gastric mucosa cells (GES-1) and human GC cells (HGC-27, SNU-5, AGS, SGC-7901, and NCI-N87) using RT-qPCR. Small RNA interference technology was used to knock down the expression of in gastric cancer cells. CCK8 solution was used to detect cell viability. Flow cytometry was used to detect apoptosis, and Western blotting was used to detect protein expression.

RESULTS

was highly expressed in GC tissues and cells, and knockdown of increased chemosensitivity to cisplatin by inducing cell apoptosis. Furthermore, promoted expression by binding to in human GC cells in vitro, and / expression was negatively related to expression, while expression was positively related to expression in human GC tissues. Moreover, overexpression of or knockdown of increased chemosensitivity to cisplatin, and knockdown of or overexpression of decreased chemosensitivity to cisplatin by inducing cell apoptosis in human GC cells. Importantly, overexpression of reduced chemosensitivity to cisplatin which increased by knockdown of , and knockdown of increased chemosensitivity to cisplatin which decreased by knockdown of in human GC cells.

CONCLUSION

The lncRNA // axis regulates cisplatin resistance in human GC cells; hence, it is a potential target for treating chemoresistance in GC.