Overexpression of miR-133 decrease primary endothelial cells proliferation and migration via FGFR1 targeting.

Zomorrod, MS and Kouhkan, F and Soleimani, M and Aliyan, A and Tasharrofi, N (2018) Overexpression of miR-133 decrease primary endothelial cells proliferation and migration via FGFR1 targeting. Exp Cell Res.

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Official URL: https://www.ncbi.nlm.nih.gov/pubmed/29608916

Abstract

Abstract Angiogenesis is one of the essential hallmarks of cancer that is controlled by the balance between positive and negative regulators. FGFR1 signaling is crucial for the execution of bFGF-induced proliferation, migration, and tube formation of endothelial cells (ECs) and onset of angiogenesis on tumors. The purpose of this study is to identify whether or not miR-133 regulates FGFR1 expression and accordingly hypothesize if it plays a crucial role in modulating bFGF/FGFR1 activity in ECs and blocking tumor angiogenesis through targeting FGFR1. The influences of miR-133 overexpression on bFGF stimulated endothelial cells were assessed by cell growth curve, MTT assaying, tube formation, and migration assays. Forced expression of miR-133 caused significant reductions in bFGF-induced proliferation and migratory ability of ECs. MiR-133 Expression was negatively correlated with both mRNA and protein levels of FGFR1 in the transfected ECs isolated from peripheral blood. Moreover, overexpression of miR-133 drastically reduced the rate of cell division and disturbed capillary network formation of transfected ECs. These findings suggest that miR-133 plays an important function in bFGF-induced angiogenesis processes in ECs and provides a rationale for new therapeutic approaches to suppress tumor angiogenesis and cancer. KEYWORDS: Angiogenesis; Cancer; FGFR1; miR-133

Item Type: Article
Subjects: R Medicine > R Medicine (General)
Divisions: Faculty of Medicine, Health and Life Sciences > School of Medicine
Depositing User: sobhan rezaiian
Date Deposited: 07 Apr 2018 20:09
Last Modified: 07 Apr 2018 20:09
URI: http://eprints.lums.ac.ir/id/eprint/1205

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