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)

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Summary

Introduction

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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