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Mini-review

Can Defective TGF-β Signaling be an Achilles Heel in Human Cancer?

David A. Foster and Noga Gadir

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Survival signals in cancer cells activate mTOR – the mammalian target of rapamycin. mTOR suppresses TGF-β signals that arrest cell cycle progression in late G1 – thus activated mTOR prevents cell cycle arrest at a checkpoint mediated by TGF-β. Rapamycin treatment resurrects TGF-β signals causing G1 arrest. Defects in TGF-β signaling are common in human cancer, and ironically, cancer cells with defective TGF-β signaling that do not arrest in G1, instead undergo apoptosis when treated with rapamycin. Thus, defective TGF-β signaling may represent an Achilles heel for rational therapeutic targeting of cancer cells using rapamycin-based strategies.

Authors

David A. Foster

Hunter College of the City University of New York

Noga Gadir

Hunter College of the City University of New York

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