Yes-associated protein gene overexpression regulated by [Formula: see text]-catenin promotes gastric cancer cell tumorigenesis

BACKGROUND: Yes-associated protein (YAP) has been reported to act as a candidate human oncogene and played a critical role in the development of multiple cancer types. OBJECTIVE: We aimed to investigate the expression, function, and underlying mechanisms of YAP in gastric cancer (GC). METHODS: Expression levels of YAP in gastric tissues were tested. CCK8 assay, clonogenic assay, apoptosis assay, transwell assay, cell scratch assay and animal study were conducted to explore the function of YAP. Chromatin immunoprecipitation (ChIP) assay and luciferase reporter assay were performed to explore the underlying mechanism. Survival analysis was carried out to reveal the relationship between YAP and clinical outcome. RESULTS: YAP was upregulated in gastric cancer tissues and correlates with poor prognosis. YAP could promote GC cells proliferation, metastatic capacity, inhibit GC cells apoptosis in vitro and in vivo. Both [Formula: see text]-catenin and YAP were mainly localized withi the tumor cell nuclei. [Formula: see text]-catenincould upregulate YAP expression by binding to the promotor region of YAP. Patients with both YAP and [Formula: see text]-catenin negetive expression had a better prognosis than others. CONCLUSIONS: YAP overexpression is driven by aberrant Wnt [Formula: see text]-catenin signalingand then contributed to the GC tumorigenesis and progression. Thus, YAP might be a potential target for GC treatment.