Id-1, a Protein Repressed by miR-29b, Facilitates the TGFβ1-Induced Epithelial-Mesenchymal Transition in Human Ovarian Cancer Cells

Background: Transforming growth factor beta 1 (TGF beta 1) 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 TGF beta 1-induced EMT in human ovarian cancer cells. Methods: Ovarian cancer cells expressing or not expressing Id-1 were incubated with TGF beta 1. 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 TGF beta 1-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 TGF beta 1-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 miR29b, facilitates TGF beta 1-induced EMT in human ovarian cancer cells and represents a promising therapeutic target for treating ovarian cancer.Copyright (C) 2014 S. Karger AG, Basel