Abstract:【Abstract】 Objective To investigate the effects of circRNAs MYLK interference on the proliferation, apoptosis, invasion and epithelialmesenchymal transformation (EMT) of endometrial carcinoma HEC1A cells and on the growth of xenograft tumors in mice. Methods MYLK-shRNAs were transfected into HEC-1A cells and MYLK interference cell model was established. The transfected HEC-1A cells were subcutaneously injected into nude mice to establish a xenograft model. In vitro experiments was grouped as Control, shRNA-NC, circMYLK- shRNA1, circMYLK-shRNA2 and circMYLK-shRNA3; in vivo experiment was grouped as shRNA-NC and circMYLK- shRNA1. The expression of MLYK was detected by RTqPCR to verify the most effective silencing sequence. The clone formation experiment detected the cell clone formation; Flow cytometry was used to detect apoptosis. Cell invasion was detected by Transwell assay. Expression of EmT-related proteins E-cadherin, N-cadherin and Vimentin were detected by Western Blot. Immunohistochemistry was used to detect the expression of Ki67 and Vimentin in tumor tissues.Results Three shRNAs interfered with MYLK and shRNA1 with the best efficiency. Compared with the control group, the clone formation rate of MYLKshrNA1 group was significantly lower (P＜0.05). The apoptosis rate was significantly increased (P＜0.05). The number of invaded cells was significantly reduced (P＜0.05). E-cadherin expression was significantly up-regulated (P＜0.05), while N-cadherin and Vimentin expression was significantly downregulated (P＜0.05). In vivo, compared with shRNA-NC, MYLK-shRNA1 significantly reduced tumor volume (P＜0.05) and tumor weight (P＜0.05). The expression of MYLK was significantly down-regulated (P＜0.05). The expression of Ki67 and Vimentin in tissues was significantly down-regulated (P＜0.05).Conclusion MYLK interference inhibited the proliferation, apoptosis, invasion and epithelialmesenchymal transformation of endometrial carcinoma HEC1A cells, and also hindered the growth of xenograft tumors in mice.
