Jin Xue-Fei, Li Hai, Zong Shi, Li Hong-Yan
Department of Urology, China-Japan Union Hospital of Jilin University, Changchun, P.R. China.
Oncol Res. 2016 Oct 27;24(6):477-485. doi: 10.3727/096504016X14685034103716.
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 β-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 β-catenin expression in RCC cells. Therefore, CTHRC1 may be a potential therapeutic target for the treatment of RCC.
含胶原蛋白三螺旋重复序列-1(CTHRC1)是一种分泌型糖蛋白,在人类癌症中经常上调。然而,CTHRC1在肾细胞癌(RCC)中的功能作用仍不清楚。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,CTHRC1在RCC组织和细胞系中上调。敲低CTHRC1可显著抑制RCC的增殖。此外,敲低CTHRC1可显著抑制RCC中的上皮-间质转化(EMT)过程,并抑制RCC细胞的迁移和侵袭。机制上,敲低CTHRC1可抑制RCC细胞中β-连环蛋白、c-Myc和细胞周期蛋白D1的表达。总之,本研究结果表明,CTHRC1下调可抑制RCC细胞的增殖、迁移、EMT和β-连环蛋白表达。因此,CTHRC1可能是治疗RCC的潜在治疗靶点。