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
- - 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 - Colorectal cancer (CRC) remains a major cause of cancer-related mortality, particularly in patients with advanced disease. Although colony stimulating factor 1 (CSF1) has been implicated in tumor progression, its role in CRC remains unclear. In this study, we showed that CSF1 was significantly upregulated in CRC tissues and cell lines, and that high CSF1 expression was associated with adverse clinicopathological features and poorer patient outcomes. Functional assays demonstrated that CSF1 promoted CRC cell proliferation, migration, invasion, and xenograft tumor growth. Importantly, CSF1 also suppressed ferroptosis, as evidenced by reduced reactive oxygen species (ROS) accumulation, lipid peroxidation, malondialdehyde (MDA) production, and Fe levels after CSF1 overexpression, whereas CSF1 knockdown produced the opposite effects. Mechanistically, CRC cells secreted CSF1, as confirmed by enzyme-linked immunosorbent assay (ELISA), and expressed colony stimulating factor 1 receptor (CSF1R), supporting a tumor-cell-intrinsic autocrine CSF1/CSF1R signaling mechanism. This autocrine signaling activated the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway, while blockade of CSF1R or inhibition of JAK/STAT3 signaling reversed CSF1-induced malignant phenotypes and ferroptosis resistance. Further rescue experiments showed that Ferrostatin-1 (Fer-1) alleviated ferroptosis induced by CSF1 knockdown or JAK/STAT3 inhibition. In addition, signal transducer and activator of transcription 3 (STAT3) overexpression upregulated glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 3 (ACSL3), linking STAT3 activation to anti-ferroptotic effector regulation. Collectively, these findings identify a tumor-cell-derived CSF1/CSF1R-JAK/STAT3 autocrine signaling axis that promotes CRC progression by suppressing ferroptosis, providing a potential therapeutic target for overcoming ferroptosis resistance in CRC. - Source: PubMed
Publication date: 2026/07/29
Shao QiuyuanXu XinyiHan XingzhiLiang ZixinZhang QunHu JingQian Xiaoping