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G-Protein Signaling Protein-17 (RGS17) Is Upregulated and Promotes Tumor Growth and Migration in Human Colorectal Carcinoma

Ling Li, He-Sheng Luo

Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, P.R. China

Oncology Research 2018, 26(1), 27-35. https://doi.org/10.3727/096504017X14900515946914

Abstract

Colorectal carcinoma is one of the leading causes of cancer-related deaths and has a high tendency for metastasis, which makes it a priority to find novel methods to diagnose and treat colorectal carcinoma at a very early stage. We studied the role of the regulator of G-protein signaling (RGS) family of proteins RGS17 in colorectal carcinoma growth and metastasis. We found that RGS17 was upregulated in both clinical colorectal carcinoma tissues and cultured colorectal carcinoma cells. Knockdown of RGS17 by specific siRNA decreased the cell proliferation rate, whereas overexpression of RGS17 with expression plasmid increased the rate in cultured cells. Consistently, a mouse model for colorectal carcinoma also showed that depletion of RGS17 significantly inhibited tumor growth in vivo. Moreover, a Transwell assay showed that RGS17 promoted the ability of colorectal carcinoma cells to migrate and invade. These data suggest that RGS17 is overexpressed in colorectal carcinoma and promotes cell proliferation, migration, and invasion.

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APA Style
Li, L., Luo, H. (2018). G-protein signaling protein-17 (RGS17) is upregulated and promotes tumor growth and migration in human colorectal carcinoma. Oncology Research, 26(1), 27-35. https://doi.org/10.3727/096504017X14900515946914
Vancouver Style
Li L, Luo H. G-protein signaling protein-17 (RGS17) is upregulated and promotes tumor growth and migration in human colorectal carcinoma. Oncol Res. 2018;26(1):27-35 https://doi.org/10.3727/096504017X14900515946914
IEEE Style
L. Li and H. Luo, "G-Protein Signaling Protein-17 (RGS17) Is Upregulated and Promotes Tumor Growth and Migration in Human Colorectal Carcinoma," Oncol. Res., vol. 26, no. 1, pp. 27-35. 2018. https://doi.org/10.3727/096504017X14900515946914



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