Abstract
Yes-associated protein (YAP) has been reported to serve an important role in gastric cancer cell survival and migration. However, the underlying mechanism remains unclear. The aim of present study was to identify the underlying mechanism through which Yap sustains gastric cancer viability and migration. The results of the present study demonstrated that YAP expression was upregulated in gastric cancer MKN-28/74 cells compared with normal gastric GES-1 cells. Functional studies revealed that silencing of YAP inhibited gastric cancer MKN-28/74 cell viability and invasion. Mechanistically, YAP may promote gastric cancer cell survival and migration/invasion by inhibiting the endoplasmic reticulum (ER) stress pathway. In addition, YAP may regulate ER stress by activating the ERK signaling pathway. The results of the present study suggested that YAP may be a tumor promoter in gastric cancer and act through the ERK/ER stress pathway; therefore, YAP may have potential implications for new approaches to gastric cancer therapy.