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

机译:G蛋白信号蛋白-17(RGS17)上调并促进人结直肠癌中的肿瘤生长和迁移

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摘要

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.
机译:结肠直肠癌是癌症相关死亡的主要原因之一,具有高趋势,使得能够在很早期诊断和治疗结肠直肠癌的新方法。我们研究了G-蛋白信号传导(RGS)蛋白质RGS17系列蛋白质的调节剂在结肠直肠癌生长和转移中的作用。我们发现RGS17在临床结肠直肠癌组织和培养结肠直肠癌细胞中上调。通过特异性siRNA的RGS17敲低降低细胞增殖率,而RGS17具有表达质粒的过度表达增加了培养细胞的速率。一致地,对直肠癌癌的小鼠模型也表明RGS17的耗尽显着抑制体内肿瘤生长。此外,Transwell测定表明RGS17促进了结直肠癌细胞迁移和侵入的能力。这些数据表明RGS17在结肠直肠癌中过表达,促进细胞增殖,迁移和侵袭。

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