Ask about this productRelated genes to: ACLY Blocking Peptide
- Gene:
- ACLY NIH gene
- Name:
- ATP citrate lyase
- Previous symbol:
- -
- Synonyms:
- ATPCL, CLATP, ACL
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-08
- Date modifiied:
- 2014-11-19
Related products to: ACLY Blocking Peptide
Related articles to: ACLY Blocking Peptide
- Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide. Current treatments offer limited efficacy and no definitive cure, underscoring the urgent need for more selective and effective therapeutic strategies. This study investigated the synthetic lethality caused by co-targeting two metabolic genes, ATP citrate lyase ( ) and oxoglutarate dehydrogenase ( ), in HCC cells. Using valproic acid (VPA) and bempedoic acid (BA) as pharmacological inhibitors of and , respectively, we observed a strong synergistic effect in inhibiting the proliferation of HCC cell lines (Hep3B and Huh7), compared to using these drugs individually. Importantly, this combination treatment exhibited little increased cytotoxicity in the non-cancerous liver cell line THLE-2, indicating a degree of selectivity. Our findings are consistent with previous reports implicating as a metabolic regulator of and in various cancers, suggesting that the inhibition of may prevent HCC cell proliferation primarily through its downstream effects on and . By directly co-targeting and , our approach may offer a more precise and safer alternative to inhibition. Additionally, while both VPA and BA have been individually associated with beneficial effects in liver disease, their combined application in the context of HCC has not been previously investigated. Limitations include the reliance on cell line models, highlighting the need for validation in more physiologically relevant systems such as human organoids and animal models. Overall, this study provides a compelling rationale for further investigation into and as a synthetic lethal pair and the therapeutic potential of the VPA-BA combination treatment in HCC. - Source: PubMed
Publication date: 2026/04/22
Manshadi Mehdi DehghanPanchal Nagesh KishanSun Lu-ZheSetoodeh PayamZare Habil - - Source: PubMed
Publication date: 2026/05/03
Zhang Yan - Cancer cells undergo intense metabolic reprogramming to provide fast proliferation, persistence, immune evasion, and resistance to therapy. Malignant cells often rely on exogenous lipids and maintaining strict metabolic regulation. Cancer cells stimulate de novo lipogenesis, lipid uptake, and storage pathways even in nutrient-limited microenvironments. This review combines current knowledge of cancer types, highlights vital enzymatic regulators and translational prospects. A comprehensive literature review was conducted, focusing on the complex relationship between lipid metabolic pathways and oncogenesis. This review focuses on de novo fatty acid synthesis, lipid uptake mechanisms, and cholesterol regulation in cancer. Important therapeutic targets, including Acetyl-CoA carboxylase (ACC), ATP citrate lyase (ACLY), fatty acid synthase (FASN), and sterol regulatory element-binding proteins (SREBPs) were evaluated. It also emphasizes the role in resistance to chemotherapy, radiotherapy, and specific targeted therapies. Several studies have revealed that dysregulated lipid metabolism contributes to tumour growth, immune evasion, and treatment resistance. Evidence from preclinical and clinical studies revealed that treatments targeting small-molecule inhibitors of FASN, ACLY, SREBPs and CD36, show promising outcomes. Alterations in lipid metabolic pathways serve as critical nodes in oncogenic networks and immune modulation. The inclusion of dietetaey modifications and nanoparticle-conjugated drug delivery provides encouraging results against tumour development. This review combines the roles of key regulators, therapeutic targets, and biomarker approaches that can update future therapies. However, challenges persist, including drug-induced toxicity, metabolic changes, and tumour heterogeneity. - Source: PubMed
Publication date: 2026/04/28
Lyle NazmunHossain Chowdhury MobaswarPramanik Krishna - Chemoresistance remains a major cause of treatment failure in colorectal cancer (CRC), yet the metabolic mechanisms sustaining efflux-mediated drug resistance are not fully defined. Here, we identify ATP-citrate lyase (ACLY) as a metabolic regulator linking citrate-dependent acetyl-CoA production to epigenetic control of MDR1/ABCB1 expression. Using genetic and pharmacologic approaches, we show that ACLY catalytic activity contributes to the maintenance of histone acetylation at H3K9 and H4K16 and supports MDR1 transcription in CRC cells. Consistently, ACLY overexpression enhances, whereas its inhibition reduces, MDR1 expression and associated resistance-related transcriptional programs. In human CRC specimens, ACLY and MDR1 levels positively correlate, with a stronger association observed in advanced-stage tumors, supporting clinical relevance of this metabolic-epigenetic axis. Metabolic tracing with C-glucose suggests that perturbation of citrate flux influences ACLY-associated pathways and acetyl-CoA availability. In this context, vitamin C treatment reduces citrate-derived acetyl-CoA and ACLY phosphorylation and is associated with global histone deacetylation and decreased MDR1 expression in vitro and in KRAS-mutant patient-derived xenografts. Together, these findings highlight ACLY-dependent acetyl-CoA production as a potential metabolic vulnerability linked to epigenetic regulation of drug efflux programs in CRC. Targeting this metabolic-chromatin axis may represent a strategy to modulate MDR1-associated chemoresistance. - Source: PubMed
Publication date: 2026/04/30
García-Bautista AnaCenigaonandia-Campillo AioraRio-Vilariño AnxoSanz-Criado LaraSelva-Giménez MartaPerez-Antolín RaquelCebrián AranchaGarcía-García LauraFernández-Aceñero María JesúsBaños-Herraiz NataliaMozas-Vivar LorenaNúñez-Delicado EstrellaGarcía-Foncillas JesúsAguilera Óscar - Diabetic kidney disease (DKD) remains a leading cause of end-stage renal disease despite advances in glucose-, blood pressure-, and albuminuria-lowering therapies. The glucose-responsive transcription factor carbohydrate response element-binding protein (ChREBP; encoded by ) regulates glycolytic-lipogenic programs, yet its causal contribution to renal injury is challenging to disentangle in advanced DKD, where bulk kidney transcriptomes reflect tissue remodeling and cellular compositional shifts. - Source: PubMed
Publication date: 2026/04/15
Liu MingliangChen ShihangWu ShiSun BeiChen Liming