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Overexpression of Csk-binding protein contributes to renal cell carcinogenesis

机译：Csk结合蛋白的过表达促进肾细胞癌变

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摘要

C-terminal Src kinase (Csk)-binding protein (Cbp) is a transmembrane adaptor protein that localizes exclusively in lipid rafts, where it regulates Src family kinase (SFK) activities through recruitment of Csk. Although SFKs are well known for their involvement in cancer, the function of Cbp in carcinogenesis remains largely unknown. In this study, we reported overexpression of Cbp in more than 70% of renal cell carcinoma (RCC) specimens and in the majority of tested RCC cell lines. Depletion of Cbp in RCC cells by RNA interference led to remarkable inhibition of cell proliferation, migration, anchorage-independent growth as well as tumorigenicity in nude mice. Strikingly, silencing of Cbp negatively affected the sustaining of Erk1/2 activation but not c-Src activation induced by serum. Besides, the RhoA activity in RCC cells was remarkably impaired when Cbp was knocked down. Overexpression of wild-type Cbp, but not its mutant Cbp/ΔCP lacking C-terminal PDZ-binding motif, significantly enhanced RhoA activation and cell migration of RCC cells. These results provided new insights into the function of Cbp in modulating RhoA activation, by which Cbp might contribute to renal cell carcinogenesis.
机译：C端Src激酶（Csk）结合蛋白（Cbp）是一种跨膜衔接蛋白，仅定位在脂质筏中，在那里它通过募集Csk来调节Src家族激酶（SFK）的活性。尽管SFK因其参与癌症而闻名，但Cbp在致癌作用中的功能仍然未知。在这项研究中，我们报道了超过70％的肾细胞癌（RCC）标本和大多数测试的RCC细胞系中Cbp的过表达。 RNA干扰使RCC细胞中的Cbp耗竭，从而显着抑制了细胞增殖，迁移，锚定非依赖性生长以及裸鼠的致瘤性。令人惊讶的是，Cbp沉默对血清诱导的Erk1 / 2激活的维持产生负面影响，但对c-Src激活没有负面影响。此外，当敲除Cbp时，RCC细胞中的RhoA活性显着受损。野生型Cbp的过表达，但缺少缺乏C端PDZ结合基序的突变型Cbp /ΔCP，则显着增强了RCC细胞的RhoA活化和细胞迁移。这些结果为Cbp在调节RhoA激活中的功能提供了新的见解，据此Cbp可能有助于肾细胞癌变。

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