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Knockdown of Collagen Triple Helix Repeat Containing-1 Inhibits the Proliferation and Epithelial-to-Mesenchymal Transition in Renal Cell Carcinoma Cells

机译:击倒含有1的胶原三螺旋重复抑制肾细胞癌细胞的增殖和上皮到间质转化。

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Collagen triple helix repeat containing-1 (CTHRC1), a secreted glycoprotein, is frequently upregulated in human cancers. However, the functional role of CTHRC1 in renal cell carcinoma (RCC) remains unclear. Thus, the aim of this study was to explore the role of CTHRC1 in RCC. Our results demonstrated that CTHRC1 was upregulated in RCC tissues and cell lines. Knockdown of CTHRC1 significantly inhibits the proliferation in RCCs. Furthermore, knockdown of CTHRC1 significantly inhibited the epithelial-to-mesenchymal transition (EMT) process in RCCs, as well as suppressed RCC cell migration and invasion. Mechanistically, knockdown of CTHRC1 inhibited the expression of beta-catenin, c-Myc, and cyclin D1 in RCC cells. In conclusion, the results of the present study indicated that CTHRC1 downregulation inhibited proliferation, migration, EMT, and beta-catenin expression in RCC cells. Therefore, CTHRC1 may be a potential therapeutic target for the treatment of RCC.
机译:含胶原蛋白三螺旋重复序列-1(CTHRC1)是一种分泌的糖蛋白,在人类癌症中经常被上调。然而,尚不清楚CTHRC1在肾细胞癌(RCC)中的功能作用。因此,本研究的目的是探讨CTHRC1在RCC中的作用。我们的结果表明,RCH组织和细胞系中CTHRC1上调。抑制CTHRC1可以显着抑制RCC中的增殖。此外,CTHRC1的敲低显着抑制了RCC中的上皮-间质转化(EMT)过程,并抑制了RCC细胞的迁移和侵袭。从机制上讲,敲低CTHRC1会抑制RCC细胞中β-catenin,c-Myc和cyclin D1的表达。总之,本研究的结果表明CTHRC1下调抑制了RCC细胞的增殖,迁移,EMT和β-catenin表达。因此,CTHRC1可能是RCC治疗的潜在治疗靶标。

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