Gab1 but not Grb2 mediates tumor progression in Met overexpressing colorectal cancer cells

Carcinogenesis
Isolde Seiden-LongMing-Sound Tsao

Abstract

Hepatocyte growth factor receptor (Met) plays an important role in the progression of multiple cancer types. The overexpression of Met in DLD-1 colon carcinoma cells with kirsten rat sarcoma oncogene homolog (KRAS) oncogene activation resulted in enhanced subcutaneous and orthotopic tumor growth rate and increased metastatic potential. To elucidate the mechanism of this effect, we stably expressed kinase-inactive Met(K1110A), Src homology 2 (SH2)-binding domain-inactive Met(Y1349/1356F), growth factor receptor-bound protein 2 (Grb2) non-binding Met(N1358H) and mutant receptors with ability to selectively recruit signaling proteins Grb2, src homology domain c-terminal adaptor homolog (Shc), phospholipase c-gamma (PLCgamma) and p85 phosphatidyl inositol 3 kinase. As subcutaneous implants, DLD-1 cells that expressed the majority of these receptor constructs failed to recapitulate the tumor growth-enhancing effect of the wild-type Met receptor. The Grb2- and Shc-recruiting Met mutants demonstrated slight but consistent tumor-suppressive activity, whereas the expression of N1358H mutant stimulated tumor growth rate comparable with the wild-type receptor. This suggests that direct Grb2/Shc binding does not contribute to the tumor pro...Continue Reading

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Citations

Jan 11, 2013·BMC Systems Biology·Meeta P PradhanMathew J Palakal
Jan 25, 2011·Cancer Biology & Therapy·Yoko MatsudaToshiyuki Ishiwata
Jun 16, 2016·The Tohoku Journal of Experimental Medicine·Lingling Hu, Ruilei Liu
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