Knockdown of Trop2 inhibits proliferation and migration and induces apoptosis of endometrial cancer cells via AKT/β-catenin pathway

Endometrial Cancer (EC) is the most common gynaecologic malignancy in western countries and has been reported to account for about 7% of female malignant tumours and 20% to 30% of female genital system malignant tumours. Accumulating evidence showed the expression of human trophoblast cell surface antigen 2 (TROP2) was abnormal in many cancers; however, the expression and role of TROP2 in EC are not clear. The TROP-2 protein expression was detected by western blot in EC cells. Cell proliferation, Apoptosis, and migration were measured by CCK-8, flow cytometry, and Transwell assay, respectively. The epithelial mesenchymal transition (EMT) and Akt/β-catenin signalling pathway-related proteins in EC cell lines were detected by western blot assay following TROP2 gene silencing. The present study revealed that the TROP2 protein was highly expressed in EC cell lines compared with human endometrial epithelial cells. The TROP2 mRNA and protein were obviously decreased following transfection with Trop2-siRNA sequence in KLE and Ishikawa cells. Meanwhile, TROP2 gene silencing in KLE and Ishikawa cells strongly inhibited cell proliferation and migration and increased cell Apoptosis. Investigation into the molecular mechanism indicated that the TROP2 gene silencing suppressed EMT and Akt/β-catenin signalling pathway activation. SIGNIFICANCE OF THE STUDY: These findings suggested that TROP2 silencing inhibited EC cell proliferation and migration and promoted cell Apoptosis. The mechanism might be related to the inhibition of the Akt/β-catenin signalling pathway in EC cells. Therefore, TROP2 may be a potential therapeutic target for the treatment of EC.