Expression of YAP in endometrial carcinoma tissues and its effect on epithelial to mesenchymal transition

BACKGROUND: Yes-associated protein (YAP) can function as a cancer suppressor or a cancer promoter. Studies have proved that YAP can collaborate with other genes to accelerate cancerous epithelial to mesenchymal transition (EMT), but little is known about how YAP performs in endometrial carcinoma (EC). METHODS: Real time-polymerase chain reaction (RT-PCR) and western blot (WB) were used to quantify the relative mRNA and protein levels of YAP in 50 EC tissue samples and 20 normal endometrial tissues in the proliferative phase. The association between YAP expression level and EC index (clinical stage, histologic grade, and lymphatic metastasis) was analyzed. YAP interference and overexpression vectors were constructed. RT-PCR and WB were used to quantify the mRNA and protein levels of YAP and EMT markers in the normal control group (N), the negative control group (NC), and the YAP interference and overexpression group. Cell counting kit-8 (CCK8) assay and scratch test were performed to evaluate the proliferation, invasion, and migration of EC cells after YAP interference and overexpression. RESULTS: The mRNA and protein levels of YAP increased in EC tissues (P<0.01) and showed differences associated with histologic grade and lymphatic metastasis, not with the clinical stage (P>0.01). CCK8 assay showed that the proliferation of EC cells was inhibited after YAP interference and increased after YAP overexpression. The cell wound healing test displayed that the migration of EC cells was inhibited after YAP interference and increased after YAP overexpression. RT-PCR and WB found the mRNA and protein levels of E-cadherin (an EMT marker) increased (P<0.01), but those of other markers (N-cadherin, Vimentin) dropped (P<0.01) after YAP interference; however, these trends were inversed after YAP overexpression (P<0.01). CONCLUSIONS: YAP serves as an EC-promoting gene that may regulate the EMT and other EC-related processes via promoting the proliferation, invasion, and migration of EC cells.