作者: Valeria C. Grossoni , Laura B. Todaro , Marcelo G. Kazanietz , Elisa D. Bal de Kier Joffé , Alejandro J. Urtreger
DOI: 10.1007/S10549-008-0299-4
关键词: Tumor progression 、 Protein kinase C 、 Cell growth 、 Cancer 、 Immunology 、 Protein Kinase C-epsilon 、 Biology 、 Metastasis 、 Fibronectin 、 Primary tumor 、 Cancer research
摘要: In this paper we investigated whether protein kinase C (PKC) β1 and PKCe, members of the classical novel PKC family, respectively, induce phenotypic alterations that could be associated with tumor progression metastatic dissemination in a murine model breast cancer. Stable overexpression PKCβ1 LM3 cells altered their ability to proliferate, adhere, survive, impaired tumorigenicity capacity. Moreover, induced re-expression fibronectin, an extracellular matrix glycoprotein which loss has been acquisition transformed phenotype different cell models, exerted important inhibition on proteases production, effects probably impact invasiveness dissemination. Conversely, PKCe enhanced survival, anchorage-independent growth, caused significant increase spontaneous lung metastasis. Our results suggest functions as inhibitory for growth metastasis whereas drives without affecting primary growth.