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G 蛋白信号转导蛋白 17（RGS17）在人结直肠癌中上调并促进肿瘤生长和迁移。

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

机构信息

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

出版信息

Oncol Res. 2018 Jan 19;26(1):27-35. doi: 10.3727/096504017X14900515946914. Epub 2017 Mar 23.

DOI:10.3727/096504017X14900515946914
PMID:28337960
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7844555/
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.

摘要

结直肠癌是癌症相关死亡的主要原因之一，并且具有很高的转移倾向，因此优先寻找新的方法来在非常早期阶段诊断和治疗结直肠癌。我们研究了 G 蛋白信号调节因子（RGS）家族蛋白 RGS17 在结直肠癌生长和转移中的作用。我们发现 RGS17 在临床结直肠癌组织和培养的结直肠癌细胞中均上调。特异性 siRNA 敲低 RGS17 会降低细胞增殖率，而表达质粒过表达 RGS17 则会增加培养细胞中的增殖率。一致地，结直肠癌的小鼠模型也表明，RGS17 的耗竭显著抑制体内肿瘤生长。此外，Transwell 测定表明 RGS17 促进了结直肠癌细胞的迁移和侵袭能力。这些数据表明，RGS17 在结直肠癌中过度表达，并促进细胞增殖、迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/1b95626dc9c5/OR-26-027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/8b88f4434784/OR-26-027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/07ee92ca72e4/OR-26-027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/b4cd1160c2ed/OR-26-027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/b13eec704670/OR-26-027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/b972224b1840/OR-26-027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/1b95626dc9c5/OR-26-027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/8b88f4434784/OR-26-027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/07ee92ca72e4/OR-26-027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/b4cd1160c2ed/OR-26-027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/b13eec704670/OR-26-027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/b972224b1840/OR-26-027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9171/7844555/1b95626dc9c5/OR-26-027-g006.jpg

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