UCHL1 Promotes Epithelial–Mesenchymal Transition Through E-Cadherin and N-Cadherin Switch in Endometrial Cancer

Objective: Endometrial cancer (EC) is one of the most common cancers in women, and its incidence is increasing worldwide. The prognosis of recurrent and advanced cancer remains poor because treatment options are limited. Ubiquitin C-terminal hydrolase-L1 (UCHL1) is associated with the progression of several cancers including EC. In this study, we analyzed the function of UCHL1 in EC progression. Methods: UCHL1 expression in the serum of patients with EC was measured using an enzyme-linked immunosorbent assay. Changes in cell migration and invasion were analyzed in UCHL1-overexpressing or UCHL1-knockdown cells (UCHL1-OE/UCHL1-KD) using wound-healing and transwell assays. Messenger RNA expression of epithelial–mesenchymal transition (EMT)-related genes in each cell was detected using quantitative real-time polymerase chain reaction (qRT-PCR). UCHL1 and EMT marker proteins were detected with Western blotting and an immunofluorescence assay (IFA). Results: Serum UCHL1 expression was significantly elevated in patients with metastases. Wound-healing assays and transwell assays showed that UCHL1 could promote cell migration and invasion. These effects were suppressed by UCHL1 knockdown and inhibition. UCHL1 overexpression modulated the expressions of EMT-related molecules in EC cells at the mRNA and protein levels. Furthermore, IFA analysis showed that changes in EMT-related molecules were consistent with lesions of UCHL1 expression. Conclusions: This study revealed that UCHL1 could contribute to promoting cell migration and invasion. These results may be associated with EMT regulation in EC cells.