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Nuclear cGAS governs transcription to control lipid metabolism, tumor growth, and therapy response
Yu Deng, Matthew J. Niederhuber, Zhichuan Zhu, Austin J. Hepperla, Le Yu, Quentin Hahn, Joshua Hartsell, Tooba Rashid, Piotr A. Mieczkowski, Hemant Kelkar, Jeremy M. Simon, Yanqiong Zhang, Alessandra Livraghi-Butrico, Meredith J. Zeller, Joseph G.C. Kennedy, Jazmin F. DePriest, Jiong Li, Yan Zhang, Xing Qiu, H. Ümit Kaniskan, Jian Jin, Corbin D. Jones, Laura E. Herring, Douglas H. Phanstiel, Xiaojing Liu, Jesse R. Raab, Brian D. Strahl, Pengda Liu
Yu Deng, Matthew J. Niederhuber, Zhichuan Zhu, Austin J. Hepperla, Le Yu, Quentin Hahn, Joshua Hartsell, Tooba Rashid, Piotr A. Mieczkowski, Hemant Kelkar, Jeremy M. Simon, Yanqiong Zhang, Alessandra Livraghi-Butrico, Meredith J. Zeller, Joseph G.C. Kennedy, Jazmin F. DePriest, Jiong Li, Yan Zhang, Xing Qiu, H. Ümit Kaniskan, Jian Jin, Corbin D. Jones, Laura E. Herring, Douglas H. Phanstiel, Xiaojing Liu, Jesse R. Raab, Brian D. Strahl, Pengda Liu
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Research Article Cell biology Metabolism Oncology

Nuclear cGAS governs transcription to control lipid metabolism, tumor growth, and therapy response

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Abstract

Cyclic GMP-AMP synthase (cGAS) is a cytosolic DNA sensor critical for host defense against microbial infections. To prevent aberrant activation, nuclear cGAS is restrained by nucleosome tethering or by barrier-to-autointegration factor–mediated restriction of its access to DNA. However, its physiological roles beyond enzymatic suppression in the nucleus remain poorly understood. Here, we present a genome-wide map of cGAS chromatin localization in human cells and unexpectedly find its binding beyond nucleosome tethering, where cGAS is recruited to chromatin by AP-1 transcription factors via a potentially previously uncharacterized transactivation domain. Integrated CUT&RUN, RNA-seq, and metabolomics analyses reveal that cGAS transcriptionally regulates cholesterol homeostasis. Mechanistically, cGAS promotes LGALS3 transcription, which inhibits ACAA2 activity to suppress fatty acid oxidation and acetyl-CoA production, thereby lowering intracellular cholesterol levels. Reduced cholesterol lowers plasma membrane phosphatidylinositol [3,4,5] triphosphate [PI(3,4,5)P3] levels and decreases mTOR complex 2 (mTORC2) activation. In contrast, cGAS depletion results in cholesterol accumulation and elevated PI(3,4,5)P3, driving mTORC2/Akt signaling, promoting xenografted tumor growth, and conferring resistance to DNA-damaging agents. In vivo, the elevated hepatic cholesterol levels observed in cGas–/– mice were largely reversed by inhibition of Akt but not STING, whereas cGAS deficiency had minimal effects on lung physiology. Collectively, our findings uncover an unexpected role for nuclear cGAS in orchestrating a transcriptional program that links lipid metabolism to cell proliferation, stress response, and cholesterol homeostasis in liver.

Authors

Yu Deng, Matthew J. Niederhuber, Zhichuan Zhu, Austin J. Hepperla, Le Yu, Quentin Hahn, Joshua Hartsell, Tooba Rashid, Piotr A. Mieczkowski, Hemant Kelkar, Jeremy M. Simon, Yanqiong Zhang, Alessandra Livraghi-Butrico, Meredith J. Zeller, Joseph G.C. Kennedy, Jazmin F. DePriest, Jiong Li, Yan Zhang, Xing Qiu, H. Ümit Kaniskan, Jian Jin, Corbin D. Jones, Laura E. Herring, Douglas H. Phanstiel, Xiaojing Liu, Jesse R. Raab, Brian D. Strahl, Pengda Liu

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Figure 7

cGAS-driven transcription of LGALS3 inhibits ACAA2 activity, suppressing fatty acid oxidation.

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cGAS-driven transcription of LGALS3 inhibits ACAA2 activity, suppressing...
(A) A list of LGALS3-binding proteins from BioGRID. (B) Representative confocal immunofluorescence (IF) images for ACAA2 and LGALS3 in MDA-MB-231 cells. (C and D) IB analysis of pulldowns and inputs using indicated bacterially purified recombinant proteins. (E and F) Representative acetyl-CoA ELISAs measuring acetyl-CoA levels in either in vitro ACAA2 reactions with recombinant LGALS3 proteins (E) or indicated MDA-MB-231 cells (F). (G) Normalized levels of [13C2]-citrate (citrate M+2) and [13C16]-palmityl-carnitine in indicated MDA-MB-231 cells relative to parental cells. Data are shown as individual values with mean, n = 2 independent biological replicates. No statistical analysis was performed because n < 3. (H) A heatmap quantifying indicated metabolites in indicated MDA-MB-231 cells with 13C-palmitate tracing for 2 hours. HP, hexose phosphate; FBP, fructose bisphosphate; DHAP/GAP, dihydroxyacetone phosphate/glyceraldehyde-3-phosphate; 2PG/3PG, 2-phosphoglycerate/3-phosphoglycerate; PEP, phosphoenolpyruvate. (I) Representative Filippin III staining images for free cholesterol in indicated MDA-MB-231 cells. Where indicated, 5 μM lovastatin was used to treat cells for 6 hours prior to staining.

Copyright © 2026 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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