Research ArticleCancer

Differential Requirement of mTOR in Postmitotic Tissues and Tumorigenesis

See allHide authors and affiliations

Sci. Signal.  27 Jan 2009:
Vol. 2, Issue 55, pp. ra2
DOI: 10.1126/scisignal.2000189

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

Blocking mTor Signals

The mammalian target of rapamycin (mTOR), a protein kinase critical to cell growth and proliferation, functions as part of two distinct multiprotein complexes. mTOR signaling is frequently disrupted in cancer; however pharmacological suppression of mTOR complex 1 (mTORC1) signaling has been of limited therapeutic efficacy. Nardella et al. show that, whereas conditional inactivation of mTOR activity (abrogating signaling through both complexes) has little effect in the adult mouse prostate, it markedly suppresses prostate cancer associated with loss of the tumor suppressor PTEN. Thus, mTOR inhibitors that target its catalytic activity may be more effective in cancer therapy than those that specifically inhibit signaling mediated through mTORC1.