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Fatty Acid Oxidation Mediated by Acyl-CoA Synthetase Long Chain 3 Is Required for Mutant KRAS Lung Tumorigenesis.

Abstract：

:KRAS is one of the most commonly mutated oncogenes in human cancer. Mutant KRAS aberrantly regulates metabolic networks. However, the contribution of cellular metabolism to mutant KRAS tumorigenesis is not completely understood. We report that mutant KRAS regulates intracellular fatty acid metabolism through Acyl-coenzyme A (CoA) synthetase long-chain family member 3 (ACSL3), which converts fatty acids into fatty Acyl-CoA esters, the substrates for lipid synthesis and β-oxidation. ACSL3 suppression is associated with depletion of cellular ATP and causes the death of lung cancer cells. Furthermore, mutant KRAS promotes the cellular uptake, retention, accumulation, and β-oxidation of fatty acids in lung cancer cells in an ACSL3-dependent manner. Finally, ACSL3 is essential for mutant KRAS lung cancer tumorigenesis in vivo and is highly expressed in human lung cancer. Our data demonstrate that mutant KRAS reprograms lipid homeostasis, establishing a metabolic requirement that could be exploited for therapeutic gain.

journal_name

Cell Rep

journal_title

Cell reports

authors

Padanad MS,Konstantinidou G,Venkateswaran N,Melegari M,Rindhe S,Mitsche M,Yang C,Batten K,Huffman KE,Liu J,Tang X,Rodriguez-Canales J,Kalhor N,Shay JW,Minna JD,McDonald J,Wistuba II,DeBerardinis RJ,Scaglioni PP

doi

10.1016/j.celrep.2016.07.009

subject

Has Abstract

pub_date

2016-08-09 00:00:00

pages

1614-1628

issue

6

issn

2211-1247

pii

S2211-1247(16)30895-6

journal_volume

16

pub_type

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