Ask about this productRelated genes to: ACSL3 Blocking Peptide
- Gene:
- ACSL3 NIH gene
- Name:
- acyl-CoA synthetase long chain family member 3
- Previous symbol:
- FACL3
- Synonyms:
- ACS3, PRO2194
- Chromosome:
- 2q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2019-03-21
Related products to: ACSL3 Blocking Peptide
Related articles to: ACSL3 Blocking Peptide
- Previous work has indicated that lipid metabolic reprogramming plays a critical role in gastric cancer (GC) development, yet the underlying molecular mechanisms remain largely undefined. In the present study, we identified a novel lipid metabolism-associated long non-coding RNA, 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1 (lncHMGCS1), which is aberrantly upregulated in GC tissues and cell lines. Functional assays demonstrated that lncHMGCS1 overexpression could promote intracellular lipid droplet accumulation, elevate the triglyceride, total cholesterol, and low-density lipoprotein cholesterol levels, and enhance GC cell proliferation. Mechanistically, lncHMGCS1 can suppress expression of miR-18b-5p, a microRNA that directly targets both lncHMGCS1 and acyl-CoA synthetase long-chain family member 3 (ACSL3). ACSL3 knockdown reversed the oncogenic effects of lncHMGCS1 on GC cells in a miR-18b-5p-dependent manner, highlighting the critical role of the lncHMGCS1-ACSL3 axis in lipid metabolic reprogramming. Collectively, our findings establish lncHMGCS1 as a driver of lipid metabolism and tumorigenesis in GC, laying the groundwork for the development of novel diagnostic and therapeutic targets for managing this disease. - Source: PubMed
Publication date: 2026/09/10
Yang QiangHe YuyangWang LejiaYuan XiaoxiaZhang JingpingChen JinxinJiang GuohuiMa WenrongLu XingtongWei ChenZhang BinDeng ShihaoLuo YaominXiao YangLong KexunXu ChaoyingYin XinqiangJiang Zhen - - Source: PubMed
Publication date: 2026/09/04
Mo QiongNing Yun-Jia - Lipids serve as both metabolic substrates and signaling mediators that critically regulate immune cell fate, function, tolerance, and intercellular communication. In hepatocellular carcinoma (HCC), it remains unclear how intratumoral linoleic acid (LA) allocation between desaturation and oxidative catabolism influences immunometabolic remodeling and post-transplant recurrence. - Source: PubMed
Publication date: 2026/08/11
Zhang RuixinZhang AnhongGao TianZhang ChengjieLiu YiqianLiu Lixin - Platinum-based chemotherapy resistance remains a major obstacle in gastric cancer (GC) treatment. Through integrated transcriptomic profiling of cisplatin-resistant xenografts and pharmacogenomic interrogation of the NCI-60 dataset, we identified Prohibitin-2 (PHB2) as a previously unrecognized determinant of chemoresistance. PHB2 was consistently upregulated in resistant tumors and associated with poor clinical outcomes. Mechanistically, PHB2 binds the lipid-metabolic enzyme ACSL3 through a defined AMP-binding-domain interface (residues W244/H254/E260), enhancing ACSL3 activity to promote monounsaturated fatty acid incorporation into phospholipids. This phospholipid remodeling suppresses lipid peroxidation and establishes a ferroptosis-resistant state. Structure-based virtual screening of an FDA-approved drug library nominated the CXCR4 antagonist Mavorixafor as a potent inhibitor of the PHB2-ACSL3 interaction. Mavorixafor disrupted lipid remodeling, restored ferroptosis susceptibility, and resensitized cisplatin-resistant GC in cell line-derived xenografts (CDOs) and patient-derived organoids (PDOs). The therapeutic effect was abrogated by the ferroptosis inhibitor Liproxstatin-1, confirming ferroptosis dependence. Collectively, our findings define a PHB2-ACSL3 lipid-metabolic axis that drives ferroptosis escape and identify Mavorixafor repurposing as an immediately translatable strategy to overcome cisplatin resistance in treatment-refractory GC. - Source: PubMed
Publication date: 2026/08/21
Xu LiangXiang WanyingWang XinyuePan YueGao JingYang JiezhenWang YufeiZhu ZhipuTong ManJin LeiYe Yan - Cerebral ischemia-reperfusion injury (CIRI) is a key contributor to stroke-related neurological damage, but the functional interplay between autophagy and ferroptosis-two critical pathological processes-remains poorly understood. - Source: PubMed
Publication date: 2026/08/09
Yang YueqingZhao MingFeng YiboYu HongliGong YuanxinLiu Qingqing