Glutamine, MTOR and autophagy: a multiconnection relationship

Cancer cells metabolize glutamine mostly through glutaminolysis, a metabolic pathway that activates MTORC1. The AMPK-MTORC1 signaling axis is a key regulator of cell growth and proliferation. Our recent investigation identified that the connection between glutamine and AMPK is not restricted to glut...

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Bibliographic Details
Published in:Autophagy 2022-11, Vol.18 (11), p.2749-2750
Main Authors: Bodineau, Clément, Tomé, Mercedes, Murdoch, Piedad del Socorro, Durán, Raúl V.
Format: Article
Language:English
Subjects:
AMP-Activated Protein Kinases
ASNS
Autophagic Puncta
Autophagy
GABA-shunt
gamma-Aminobutyric Acid
glutamine
Glutamine - metabolism
glutamoptosis
Mechanistic Target of Rapamycin Complex 1 - metabolism
MTORC1
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Summary:Cancer cells metabolize glutamine mostly through glutaminolysis, a metabolic pathway that activates MTORC1. The AMPK-MTORC1 signaling axis is a key regulator of cell growth and proliferation. Our recent investigation identified that the connection between glutamine and AMPK is not restricted to glutaminolysis. Rather, we demonstrated the crucial role of ASNS (asparagine synthetase (glutamine-hydrolyzing)) and the GABA shunt for the metabolic control of the AMPK-MTORC1 axis during glutamine sufficiency. Our results elucidated a metabolic network by which glutamine metabolism regulates the MTORC1-macroautophagy/autophagy pathway through two independent branches involving glutaminolysis and ASNS-GABA shunt. Abbreviations: αKG: alpha-ketoglutarate; AMPK: AMP-activated protein kinase; ASNS: asparagine synthetase (glutamine-hydrolyzing); GLUD/GDH: glutamate dehydrogenase; GLS: glutaminase; GOT1: glutamic-oxaloacetic transaminase 1; MTORC1: mechanistic target of rapamycin kinase complex 1; TCA: tricarboxylic acid.
ISSN:1554-8627
1554-8635
DOI:10.1080/15548627.2022.2062875