Yue Teng1, Le Zhao, Yan Zhang, Wei Chen, Xu Li. 1. Center for Translational Medicine, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, PR China.
Abstract
BACKGROUND: Transforming growth factor beta 1 (TGFβ1) can induce epithelial-mesenchymal transition (EMT) in various human cancers, but the complex mechanisms underlying this have not been fully elucidated. Inhibitor of DNA binding 1 (Id-1) has been identified as a novel marker of ovarian cancer progression. This study aims to investigate the role of Id-1 in TGFβ1-induced EMT in human ovarian cancer cells. METHODS: Ovarian cancer cells expressing or not expressing Id-1 were incubated with TGFβ1. Changes in the EMT markers E-cadherin, vimentin, N-cadherin, Id-1, and miR-29b were detected using western blotting and qPCR analyses. Wound healing, transwell migration, and invasion assays were performed in cells where Id-1 was either knocked down or overexpressed. The effects of transfecting miR-29b mimics and inhibitors on Id-1 mRNA and protein expression were assessed. The interaction between miR-29b and Id-1 was confirmed using a luciferase reporter assay. RESULTS: Id-1 expression was increased and miR-29b expression was repressed in TGFβ1-responsive ovarian cancer cells. Id-1 overexpression increases and Id-1 knockdown decreases cell migration and invasion capacities. Id-1 silencing leads to a partial blocking of TGFβ1-induced EMT. miR-29b negatively regulates Id-1 expression. Direct binding of miR-29b to the 3'UTR region of Id-1 was confirmed using a luciferase reporter assay. CONCLUSION: Id-1, a protein repressed by miR-29b, facilitates TGFβ1-induced EMT in human ovarian cancer cells and represents a promising therapeutic target for treating ovarian cancer.
BACKGROUND:Transforming growth factor beta 1 (TGFβ1) can induce epithelial-mesenchymal transition (EMT) in various humancancers, but the complex mechanisms underlying this have not been fully elucidated. Inhibitor of DNA binding 1 (Id-1) has been identified as a novel marker of ovarian cancer progression. This study aims to investigate the role of Id-1 in TGFβ1-induced EMT in humanovarian cancer cells. METHODS:Ovarian cancer cells expressing or not expressing Id-1 were incubated with TGFβ1. Changes in the EMT markers E-cadherin, vimentin, N-cadherin, Id-1, and miR-29b were detected using western blotting and qPCR analyses. Wound healing, transwell migration, and invasion assays were performed in cells where Id-1 was either knocked down or overexpressed. The effects of transfecting miR-29b mimics and inhibitors on Id-1 mRNA and protein expression were assessed. The interaction between miR-29b and Id-1 was confirmed using a luciferase reporter assay. RESULTS:Id-1 expression was increased and miR-29b expression was repressed in TGFβ1-responsive ovarian cancer cells. Id-1 overexpression increases and Id-1 knockdown decreases cell migration and invasion capacities. Id-1 silencing leads to a partial blocking of TGFβ1-induced EMT. miR-29b negatively regulates Id-1 expression. Direct binding of miR-29b to the 3'UTR region of Id-1 was confirmed using a luciferase reporter assay. CONCLUSION:Id-1, a protein repressed by miR-29b, facilitates TGFβ1-induced EMT in humanovarian cancer cells and represents a promising therapeutic target for treating ovarian cancer.
Authors: Ling Zhao; Linjuan Huang; Jing Zhang; Jiaming Fan; Fang He; Xia Zhao; Hao Wang; Qing Liu; Deyao Shi; Na Ni; William Wagstaff; Mikhail Pakvasa; Kai Fu; Andrew B Tucker; Connie Chen; Russell R Reid; Rex C Haydon; Hue H Luu; Le Shen; Hongbo Qi; Tong-Chuan He Journal: Am J Transl Res Date: 2020-12-15 Impact factor: 4.060
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