Abstract
ABSTRACTA master promoter of cell growth, mammalian target of rapamycin (mTOR) is upregulated in a large percentage of cancer cells. Still, targeting mTOR using rapamycin has a limited outcome in patients. Our recent results highlight the additional role of mTOR as a tumor suppressor, explaining these modest results in the clinic.
Highlights
The serine/threonine kinase mammalian target of rapamycin is a central regulator of mammalian cell growth. mTOR forms 2 complexes, termed mTOR complex 1 and mTOR complex 2. While both complexes are stimulated by growth factors, only mTORC1 can be activated by amino acids (1Cell Res)
Our work revealed an unexpected mechanism by which the unbalanced activation of glutaminolysis in the absence of other amino acids induces a particular type of mTORC1-dependent cell death that we are naming “glutamoptosis” (3Nat Comm)
The most accepted reason is the existence of a negative feedback loop downstream of mTORC1 which, upon its inhibition, upregulates the phosphoinositide 3-kinase (PI3K) signaling (8Curr Biol)
Summary
A master promoter of cell growth, mammalian target of rapamycin (mTOR) is upregulated in a large percentage of cancer cells. KEYWORDS a-ketoglutarate; autophagy; cancer metabolism; glutamoptosis; mTORC1; rapamycin The serine/threonine kinase mammalian target of rapamycin (mTOR) is a central regulator of mammalian cell growth.
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