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.
journal_name
Carcinogenesisjournal_title
Carcinogenesisauthors
Samoylenko A,Vynnytska-Myronovska B,Byts N,Kozlova N,Basaraba O,Pasichnyk G,Palyvoda K,Bobak Y,Barska M,Mayevska O,Rzhepetsky Y,Shuvayeva H,Lyzogubov V,Usenko V,Savran V,Volodko N,Buchman V,Kietzmann T,Drobot Ldoi
10.1093/carcin/bgs228subject
Has Abstractpub_date
2012-10-01 00:00:00pages
1976-84issue
10eissn
0143-3334issn
1460-2180pii
bgs228journal_volume
33pub_type
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