ArticleProceedings of the National Academy of Sciences of the United States of America2024
ACSL4-mediated H3K9 and H3K27 hyperacetylation upregulates SNAIL to drive TNBC metastasis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Mitochondrial dynamics: A promising tool for personalized TNBC management.Genes & diseases · 2026Review
- Inhibition of Acetylation Activity of p300/CBP Ameliorates Hepatic Steatosis Through Downregulation of ACSL4.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- Disruption of macrophage migration inhibitory factor signaling induces major tumor-associated macrophage phenotypes in human M2 macrophages.Molecular biomedicine · 2026Article
- Adipocyte-rich microenvironment promotes TNBC progression through SIRT6-associated ACSL5 dysregulation and lipid storage-associated phenotypes.Journal of experimental & clinical cancer research : CR · 2026Article
- HCV-Induced Hepatocarcinogenesis: Molecular Mechanisms, Persistent Cancer Risk, and Future Perspectives.Biomedicines · 2026Review
- Epigenetic regulation of ACSL4 via H2A monoubiquitylation connects lipid metabolism to BAP1-mediated ferroptosis.Cell death and differentiation · 2026Article
- Identification and Prognostic Analysis of Immune-Related Genes Co-Regulated by Key Histone Modifications in Breast Cancer.Current issues in molecular biology · 2026Article
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- Arginine methylation of human DNA topoisomerase I by PRMT5 facilitates DNA relaxation.Nucleic acids research · 2026Article
- PDK4-driven metabolic reprogramming enhances mesothelial cell invasion in colorectal cancer peritoneal metastasis.Acta biochimica et biophysica Sinica · 2026Article
- Metabolic reprogramming-driven resistance to multi-kinase inhibitors in hepatocellular carcinoma: molecular mechanisms and therapeutic opportunities.Molecular cancer · 2026Review
- Antitumor effects of Santalol on non-small cell lung cancer via disruption of NF-κB-mediated lipid metabolism.Journal of translational medicine · 2026Article
- Intratumoral Heterogeneity of MAGED4 Expression in Oral Squamous Cell Carcinoma: Epigenetic Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2025Article
- 5'-Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation-Mediated PAK2 Upregulation to Promote Cadmium-Induced Breast Cancer Progression by Impairing Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Construction of the bromodomain-containing protein-associated prognostic model in triple-negative breast cancer.Cancer cell international · 2025Article
- Iron-fueled ferroptosis: a new axis for immunomodulation to overcome cancer drug resistance-from immune microenvironment crosstalk to therapeutic translation.Frontiers in immunology · 2025Review
- ACSL4-mediated H3K9 and H3K27 hyperacetylation upregulates SNAIL to drive TNBC metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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19 authors.
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Abstract
Triple-negative breast cancer (TNBC) has profound unmet medical need globally for its devastating clinical outcome associated with rapid metastasis and lack of targeted therapies. Recently, lipid metabolic reprogramming especially fatty acid oxidation (FAO) has emerged as a major driver of breast cancer metastasis. Analyzing the expression of major FAO regulatory genes in breast cancer, we found selective overexpression of acyl-CoA synthetase 4 (ACSL4) in TNBC, which is primarily attributed to the absence of progesterone receptor. Loss of ACSL4 function, by genetic ablation or pharmacological inhibition significantly reduces metastatic potential of TNBC. Global transcriptome analysis reveals that ACSL4 activity positively influences the gene expression related to TNBC migration and invasion. Mechanistically, ACSL4 modulates FAO and intracellular acetyl-CoA levels, leading to hyperacetylation of particularly H3K9ac and H3K27ac marks resulting in overexpression of SNAIL during the course of TNBC metastatic spread to lymph node and lung. Further, human TNBC metastasis exhibits positive correlation among ACSL4, H3K9ac, H3K27ac, and SNAIL expression. Altogether, our findings provide molecular insights regarding the intricate interplay between metabolic alterations and epigenetic modifications, intertwined to orchestrate TNBC metastasis, and posit a rational understanding for the development of ACSL4 inhibitors as a targeted therapy against TNBC.
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