Yes-associated protein gene overexpression regulated by β-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. Bothβ-catenin and YAP were mainly localized withi the tumor cell nuclei. β-catenincould upregulate YAP expression by binding to the promotor region of YAP. Patients with both YAP and β-catenin negetive expression had a better prognosis than others.

CONCLUSIONS

YAP overexpression is driven by aberrant Wnt β-catenin signalingand then contributed to the GC tumorigenesis and progression. Thus, YAP might be a potential target for GC treatment.