Chenyu Jin1, Ruojia Liang2. 1. School of Medicine International Healthcare Center, Second Affiliated Hospital Zhejiang University, HangZhou, China. 2. Department of Gynaecology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, HangZhou, China.
Abstract
AIM: AKT signaling regulates multiple biological processes and expresses in various cancers. miR-205 plays complex roles in tumorigenesis and tumor progression by acting either as a tumor suppressor or an oncogene depending on the tumor type. Here we describe the molecular mechanism of miR-205 regulating epithelial-mesenchymal transition by activation of AKT signaling in endometrial cancer cells HEC-50B and HEC-1-A. MATERIAL AND METHODS: The proliferation of HEC-50B cells transfected with miR-205 mimic was assessed by WST-1 assay. The migration and invasion were evaluated by BD transwell migration and matrigel invasion assays. The EMT markers were detected by Western blot. RESULTS: We found that miR-205 increased the proliferation in HEC-50B cells. The migration and invasion of HEC-50B cells and HEC-1-A cells were enhanced by miR-205. When HEC-50B cells and HEC-1-A cells were treated with anti-miR-205 inhibitor, the migration and invasion were decreased as compared with the negative control. The overexpression of miR-205 inhibited E-cadherin expression and promoted Snail expression by activation of AKT and downregulation of glycogen synthase kinase 3β. However, after the HEC-50B cells and HEC-1-A cells were treated with anti-miR-205 inhibitor, E-cadherin expression was increased and Snail protein level was decreased by inhibition of AKT expression. CONCLUSION: Our data strongly suggest that miR-205 plays an important role in endometrial cancer migration and invasion by targeting the AKT pathway. Our data highlight miR-205 as a potential molecular target for endometrial cancer treatment.
AIM: AKT signaling regulates multiple biological processes and expresses in various cancers. miR-205 plays complex roles in tumorigenesis and tumor progression by acting either as a tumor suppressor or an oncogene depending on the tumor type. Here we describe the molecular mechanism of miR-205 regulating epithelial-mesenchymal transition by activation of AKT signaling in endometrial cancer cells HEC-50B and HEC-1-A. MATERIAL AND METHODS: The proliferation of HEC-50B cells transfected with miR-205 mimic was assessed by WST-1 assay. The migration and invasion were evaluated by BD transwell migration and matrigel invasion assays. The EMT markers were detected by Western blot. RESULTS: We found that miR-205 increased the proliferation in HEC-50B cells. The migration and invasion of HEC-50B cells and HEC-1-A cells were enhanced by miR-205. When HEC-50B cells and HEC-1-A cells were treated with anti-miR-205 inhibitor, the migration and invasion were decreased as compared with the negative control. The overexpression of miR-205 inhibited E-cadherin expression and promoted Snail expression by activation of AKT and downregulation of glycogen synthase kinase 3β. However, after the HEC-50B cells and HEC-1-A cells were treated with anti-miR-205 inhibitor, E-cadherin expression was increased and Snail protein level was decreased by inhibition of AKT expression. CONCLUSION: Our data strongly suggest that miR-205 plays an important role in endometrial cancer migration and invasion by targeting the AKT pathway. Our data highlight miR-205 as a potential molecular target for endometrial cancer treatment.
Authors: Sanjeev K Srivastava; Aamir Ahmad; Haseeb Zubair; Orlandric Miree; Seema Singh; Rodney P Rocconi; Jennifer Scalici; Ajay P Singh Journal: Cancer Lett Date: 2017-05-24 Impact factor: 8.679
Authors: Max Michael Traeger; Jan Rehkaemper; Hansjoerg Ullerich; Konrad Steinestel; Eva Wardelmann; Norbert Senninger; Sameer Abdallah Dhayat Journal: J Cancer Res Clin Oncol Date: 2018-09-22 Impact factor: 4.553