Xizhou Lin1, Liang Zheng1, Hongliang Song2, Jun Xiao2, Bujian Pan2, Haichuan Chen2, Xiaodan Jin2, Haibo Yu3. 1. Department of Digestive Diseases, Wenzhou People's Hospital, The Third Clinical College of Wenzhou Medical University, Wenzhou 325000, PR China. 2. Department of Surgery, Wenzhou Central Hospital, The Dingli Clinical Institute of Wenzhou Medical University, Wenzhou 325000, PR China. 3. Department of Surgery, Wenzhou Central Hospital, The Dingli Clinical Institute of Wenzhou Medical University, Wenzhou 325000, PR China. Electronic address: yuhaibozjwz@163.com.
Abstract
OBJECTIVE: This study aims to explore effects of miR-183 on epithelial-mesenchymal transition (EMT) and invasion by targeting MTA1 in human pancreatic cancer (PC) cells. METHODS: Totally, 108 PC patients admitted in Wenzhou Central Hospital and Wenzhou People's Hospital, The Dingli Clinical Institute of Wenzhou Medical University from March 2010 to March 2014 were enrolled. qRT-PCR and immunohistochemistry were applied to examine expression of MTA1 mRNA and protein. Samples were divided into 6 groups: blank, NC, miR-183 mimics, miR-183 inhibitors, MTA1-siRNA and miR-183 inhibitors +MTA1-siRNA groups. CCK8 method was employed for determining cell proliferation rate, flow cytometry for cell apoptosis rate, scratch test for cell migration and Transwell assay for cell invasion. qRT-PCR and Western blotting were used to determine expression of MTA1, E-cadherin and Vimentin mRNA and protein. RESULTS: Positive expression rate of MTA1 was upregulated in PC tissues, and expression of miR-183 and MTA1 was associated with differentiation, migration, tumor size, TNM. The miR-183 mimics and MTA1-siRNA groups showed a decrease in proliferation, migration and invasion, whereas increased apoptosis, in comparison with blank and NC groups, as expression of MTA1 and Vimentin mRNA and protein were reduced, expression of E-cadherin mRNA and protein was elevated. Compared to blank and NC groups, the miR-183 inhibitors group exhibited enhanced proliferation, migration and invasion and inhibited apoptosis; increased expressions of MTA1 and Vimentin mRNA and protein and decreased expressions of E-cadherin mRNA and protein. CONCLUSION: Our study supported that miR-183 could repress EMT and invasion of human PC cells through inhibition of MTA1 expression.
OBJECTIVE: This study aims to explore effects of miR-183 on epithelial-mesenchymal transition (EMT) and invasion by targeting MTA1 in humanpancreatic cancer (PC) cells. METHODS: Totally, 108 PC patients admitted in Wenzhou Central Hospital and Wenzhou People's Hospital, The Dingli Clinical Institute of Wenzhou Medical University from March 2010 to March 2014 were enrolled. qRT-PCR and immunohistochemistry were applied to examine expression of MTA1 mRNA and protein. Samples were divided into 6 groups: blank, NC, miR-183 mimics, miR-183 inhibitors, MTA1-siRNA and miR-183 inhibitors +MTA1-siRNA groups. CCK8 method was employed for determining cell proliferation rate, flow cytometry for cell apoptosis rate, scratch test for cell migration and Transwell assay for cell invasion. qRT-PCR and Western blotting were used to determine expression of MTA1, E-cadherin and Vimentin mRNA and protein. RESULTS: Positive expression rate of MTA1 was upregulated in PC tissues, and expression of miR-183 and MTA1 was associated with differentiation, migration, tumor size, TNM. The miR-183 mimics and MTA1-siRNA groups showed a decrease in proliferation, migration and invasion, whereas increased apoptosis, in comparison with blank and NC groups, as expression of MTA1 and Vimentin mRNA and protein were reduced, expression of E-cadherin mRNA and protein was elevated. Compared to blank and NC groups, the miR-183 inhibitors group exhibited enhanced proliferation, migration and invasion and inhibited apoptosis; increased expressions of MTA1 and Vimentin mRNA and protein and decreased expressions of E-cadherin mRNA and protein. CONCLUSION: Our study supported that miR-183 could repress EMT and invasion of human PC cells through inhibition of MTA1 expression.
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