Research ArticleCancer

Dynamic Reprogramming of Signaling Upon Met Inhibition Reveals a Mechanism of Drug Resistance in Gastric Cancer

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Science Signaling  22 Apr 2014:
Vol. 7, Issue 322, pp. ra38
DOI: 10.1126/scisignal.2004839

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Met with Resistance in Gastric Cancer

The hepatocyte growth factor receptor Met is associated with poor prognosis in various cancers, but the efficacy of Met inhibitors is often impeded by resistance. By comparing transcriptional changes at multiple time points after stimulation or inhibition of Met, Lai et al. identified critical mediators of Met-induced proliferation and Met inhibitor resistance in gastric cancer cell lines. Cancer cells or tumors exposed to Met inhibitors had decreased abundance of phosphatases, and this correlated with reactivation of the pro-proliferative MEK-ERK pathway and the emergence of drug resistance. Combining Met and MEK inhibitors was more cytotoxic to gastric cancer cells in culture than was either inhibitor alone, suggesting that this combination strategy may be effective in gastric cancer.

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