Research ArticleCancer Biology

Only a Subset of Met-Activated Pathways Are Required to Sustain Oncogene Addiction

See allHide authors and affiliations

Science Signaling  08 Dec 2009:
Vol. 2, Issue 100, pp. ra80
DOI: 10.1126/scisignal.2000643

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

This article has a correction. Please see:

Addicted to Only a Few

Sometimes cancer cells become dependent on a particular aberrantly activated protein, encoded by an oncogene. Thus, inhibiting the activity of such an oncogenic protein is one approach to treating cancer. Bertotti et al. found that inhibition of the oncogenic protein Met, which caused “addicted” cells to stop proliferating, only inactivated a subset of the pathways downstream of Met. They identified a signaling and transcriptional response “signature,” involving Ras and phosphoinositide 3-kinase pathways, that contributed to cell-cycle arrest in response to Met inhibition in the Met-addicted cancer cells. A similar biochemical and transcriptional signature was found in response to inhibition of another oncogenic receptor tyrosine kinase, the epidermal growth factor receptor, in cells addicted to this second oncogene. Thus, cells addicted to oncogenic receptor tyrosine kinases may develop common mechanisms to sustain malignancy and therefore be susceptible to similar therapeutic interventions.

View Full Text

Stay Connected to Science Signaling