SynthesisCancer medicine2018
Mitochondrial Acetyl-CoA Synthetase 3 is Biosignature of Gastric Cancer Progression.
Synthesis in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Ablation of ACSS2 drives alteration to cardiac and hepatic proteomic landscapes in a tissue- and sex-specific manner.Journal of proteomics · 2026Article
- Multi-omics analysis and experiments validate the tumor-suppressive role of mitochondrial lipid metabolism gene ACSM5 in lung adenocarcinoma and its impact on the immune microenvironment.Human genomics · 2026Article
- A Proteomic Study of the Dual Oncogenic and Tumor-Suppressive Roles of SIRT3 in Lung and Breast Cancer Cell Lines.International journal of molecular sciences · 2026Article
- Exploring the significance of fatty acid metabolism reprogramming in the pathogenesis of cancer and anticancer therapy.Annals of medicine · 2025Review
- Recent advances in understanding the relationship between lipid metabolism and immune escape in the tumor microenvironment of gastric cancer.Medical review (2021) · 2025Review
- Ether-lipids accumulation promotes hepatocellular carcinoma progression linked to PPARα deficiency.Journal of biomedical science · 2025Article
- Article
- Ether-Linked Glycerophospholipids Are Potential Chemo-Desensitisers and Are Associated With Overall Survival in Carcinoma Patients.Journal of cellular and molecular medicine · 2024Article
- Comprehensive pan-cancer analysis of ACSS3 as a biomarker for prognosis and immunotherapy response.Heliyon · 2024Article
- Sex-specific survival gene mutations are discovered as clinical predictors of clear cell renal cell carcinoma.Scientific reports · 2024Article
- Lipid Metabolism as a Potential Target of Liver Cancer.Journal of hepatocellular carcinoma · 2024Review
- Lipid metabolism-related gene signatures for predicting the prognosis of lung adenocarcinoma.Translational cancer research · 2023Article
- Article
- Estradiol and Estrone Have Different Biological Functions to Induce NF-κB-Driven Inflammation, EMT and Stemness in ER+ Cancer Cells.International journal of molecular sciences · 2023Article
- Landscape of Druggable Molecular Pathways Downstream of Genomic CDH1/Cadherin-1 Alterations in Gastric Cancer.Journal of personalized medicine · 2022Article
- Lipid metabolism in pancreatic cancer: emerging roles and potential targets.Cancer communications (London, England) · 2022Review
- Metabolic changes induced by DNA damage in Ramos cells: exploring the role of mTORC1 complex.FEBS open bio · 2022Article
- Key Molecules of Fatty Acid Metabolism in Gastric Cancer.Biomolecules · 2022Review
- ACSS3 in brown fat drives propionate catabolism and its deficiency leads to autophagy and systemic metabolic dysfunction.Clinical and translational medicine · 2022Article
- Statin as a therapeutic agent in gastroenterological cancer.World journal of gastrointestinal oncology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholesterol affects cancer progression, and acetyl-CoA is the primary cholesterogenesis substrate. The previous work has defined cholesterol bioflux via lipoprotein/receptor route is the gastric cancer (GCa) prognosis biosignature. The prognosis importance of acetyl-CoA to cholesterogenesis (mevalonate pathway) in GCa is yet to be defined. Using Kaplan-Meier Plotter web-based gene survival analyzer and The Cancer Genome Atlas (TCGA)-database analyzed with DBdriver.v2 platform, we revealed acetyl-CoA production and the mevalonate pathway are associated with GCa prognosis. We found mitochondrial-derived acetyl-CoA contributing enzymes (acyl-coA synthetase super-family 3; ACSS3) is the GCa progression confounder. Interestingly, it is not HMGCR (the committee enzyme of mevalonate pathway), but lower mevalonate pathway enzymes (e.g., MVK, LSS, DHCR14A1, SC4MOL, HSD17B7, SC5D) promote GCa patients 5-years overall survival in a differential level. Advanced analyses found ACSS3 is prognosis biosignatures for multiple GCa disease conditions. This report uncovered a higher expression of ACSS3 in tumor comparing to normal parental lesions, which implicates a targeting value for GCa therapy. While knockdown ACSS3 could suppress growth and invasion of GCa cells, of which even more impactful under starvation condition. This is the first report, surprisingly, revealed ACSS3 as important cancer prognosis biomarker. Targeting ACSS3 could be a novel therapeutic strategy for cancer, in this case, GCa.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.