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BMB Rep ; 48(3): 159-65, 2015 Mar.
Article in English | MEDLINE | ID: mdl-24998263

ABSTRACT

Although the short isoform of ErbB3-binding protein 1 (Ebp1), p42 has been considered to be a potent tumor suppressor in a number of human cancers, whether p42 suppresses tumorigenesis of lung cancer cells has never been clarified. In the current study we investigated the tumor suppressor role of p42 in non-small cell lung cancer cells. Our data suggest that the expression level of p42 is inversely correlated with the cancerous properties of NSCLC cells and that ectopic expression of p42 is sufficient to inhibit cell proliferation, anchorage-independent growth, and invasion as well as tumor growth in vivo. Interestingly, p42 suppresses Akt activation and overexpression of a constitutively active form of Akt restores the tumorigenic activity of A549 cells that is ablated by exogenous p42 expression. Thus, we propose that p42 Ebp1 functions as a potent tumor suppressor of NSCLC through interruption of Akt signaling.


Subject(s)
Adaptor Proteins, Signal Transducing/physiology , Carcinoma, Non-Small-Cell Lung/metabolism , Genes, Tumor Suppressor , Lung Neoplasms/metabolism , RNA-Binding Proteins/physiology , Apoptosis , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line, Tumor , ErbB Receptors/metabolism , Humans , Lung Neoplasms/pathology , Signal Transduction
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