Research ArticleCancer

A PI3K- and GTPase-independent Rac1-mTOR mechanism mediates MET-driven anchorage-independent cell growth but not migration

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Science Signaling  23 Jun 2020:
Vol. 13, Issue 637, eaba8627
DOI: 10.1126/scisignal.aba8627

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Tumor growth and spread MET-ered by Rac

Anchorage-independent proliferation and cell migration are critical to primary tumor growth and metastatic spread. These behaviors are promoted by growth factor signaling, which is generally mediated by the kinase PI3K to downstream effectors that include the kinase mTOR and the GTPase Rac1. In both cultured cells and in tumor grafts in mice, Hervieu et al. found that anchorage-independent growth by cells expressing a mutant form of the growth factor receptor MET was mediated not by PI3K or the GTPase activity of Rac1, but rather by a noncatalytic, plasma membrane–localized interaction between Rac1 and mTOR. These findings refine our understanding of MET-driven signaling in tumor growth and may also explain why PI3K inhibitors must often be combined with mTOR inhibitors to effectively suppress tumor growth.

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