Inhibition of AGS cancer cell proliferation following siRNA-mediated downregulation of VEGFR2

Zarei Mahmudabadi, Ali. and Karimi, Masoomeh Masoomi. and Bahabadi, Majid. and Bagheri Hoseinabadi, Zahra. and JafariSani, Moslem. and Ahmadi, Reza. (2016) Inhibition of AGS cancer cell proliferation following siRNA-mediated downregulation of VEGFR2. Cell Journal, 18 (3). pp. 381-388.


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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?ow cytometry analyses of VEGFR2 expression. Results: Real-time PCR and Western blot results showed that VEGFR2 expression signifcantly 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
Additional Information: cited By 0
Uncontrolled Keywords: Apoptosis, Downregulation, SiRNA, VEGFR2
Subjects: WG Cardiovascular System
QZ pathology-Neoplasms
Divisions: Faculty of Medicine > Basic Sciences Academic Groups > Department of Biochemistry and Genetics
Depositing User: zahra bagheri .
Date Deposited: 10 Jul 2017 03:57
Last Modified: 19 Feb 2018 07:56

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