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• W2114994233 abstract "The adaptor protein regulator for ubiquitous kinase/c-Cbl-interacting protein of 85kDa (Ruk/CIN85) was found to modulate HER1/EGFR signaling and processes like cell adhesion and apoptosis. Although these features imply a role in carcinogenesis, it is so far unknown how and by which molecular mechanisms Ruk/CIN85 could affect a certain tumor phenotype. By analyzing samples from breast cancer patients, we found high levels of Ruk l /CIN85 especially in lymph node metastases from patients with invasive breast adenocarcinomas, suggesting that Ruk l /CIN85 contributes to malignancy. Expression of Ruk l /CIN85 in weakly invasive breast adenocarcinoma cells deficient of Ruk l /CIN85 indeed converted them into more malignant cells. In particular, Ruk l /CIN85 reduced the growth rate, decreased cell adhesion, enhanced anchorage-independent growth, increased motility in both transwell migration and wound healing assays as well as affected the response to epidermal growth factor. Thereby, Ruk l /CIN85 led to a more rapid and prolonged epidermal growth factor-dependent activation of Src, Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk l /CIN85-dependent changes in cell motility. Together, this study indicates that high levels of Ruk l /CIN85 contribute to the conversion of breast adenocarcinoma cells into a more malignant phenotype via modulation of the Src/Akt pathway." @default.
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• W2114994233 date "2012-07-12" @default.
• W2114994233 modified "2023-10-18" @default.
• W2114994233 title "Increased levels of the HER1 adaptor protein Ruk l /CIN85 contribute to breast cancer malignancy" @default.
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• W2114994233 doi "https://doi.org/10.1093/carcin/bgs228" @default.
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