Repository of Research and Investigative Information

Repository of Research and Investigative Information

Rafsanjan University of Medical Sciences

Inhibition of AGS Cancer Cell Proliferation following siRNA-Mediated Downregulation of VEGFR2

(2016) Inhibition of AGS Cancer Cell Proliferation following siRNA-Mediated Downregulation of VEGFR2. Cell Journal. pp. 381-388. ISSN 2228-5806

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Objective: Vascular endothelial growth factor (VEGF) and VEGF receptors (VEGFRs) play important roles in angiogenesis of different developmental mechanisms such as wound healing, embryogenesis and diseases, including different types of cancer. VEGFR2 is associated with cell proliferation, migration, and vascular permeability of endothelial cells. Blocking VEGF and its receptors is suggested as a therapeutic approach to prevent tumor growth. In this study, we aim to block VEGF signaling via small interfering RNA (siRNA) inhibition of VEGFR2. Materials and Methods: In this experimental study, we used the RNA interference (RNAi) mechanism to suppress expression of the VEGFR2 gene. We conducted the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay, real-time polymerase chain reaction (PCR), Western blot, and flow cytometry analyses of VEGFR2 expression. Results: Real-time PCR and Western blot results showed that VEGFR2 expression significantly downregulated. This suppression was followed by inhibition of cell proliferation, reduction of viability, and induction of apoptosis in the cancer cells. Conclusion: These findings suggest that VEGFR2 has a role in cell proliferation and tumor growth. Accordingly, it is suggested that VEGFR2 can be a therapeutic target for controlling tumor growth and proliferation.

Item Type: Article
Keywords: VEGFR2 Downregulation siRNA Apoptosis endothelial growth-factor herpetic stromal keratitis factor receptor-1 gastric-cancer angiogenesis pathway bevacizumab expression paclitaxel neovascularization Cell Biology
Page Range: pp. 381-388
Journal or Publication Title: Cell Journal
Journal Index: ISI
Volume: 18
Number: 3
ISSN: 2228-5806
Depositing User: مهندس مهدی شریفی

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