ArticleCancer biology & medicine2024
ACSL3 regulates breast cancer progression
Article in Cancer biology & medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed.
- Bone marrow adipose tissue: fueling breast cancer bone metastasis via pro-tumor mechanisms and novel therapeutic targets.Clinical & experimental metastasis · 2026Review
- The Crosstalk Between YAP/TAZ and Cancer Metabolism: From Mechanistic Insights to Drug Discovery.International journal of molecular sciences · 2026Review
- Opposing roles of DGAT-mediated lipid droplet biogenesis in the regulation of ferroptosis sensitivity.The FEBS journal · 2026Article
- ACSL3 inhibits ferroptosis in gastric cancer through the activation of unfolded protein response following endoplasmic reticulum stress.Cell death & disease · 2026Article
- SIRT7-mediated ACSL3 delactylation suppresses colorectal cancer progression by orchestrating tumor-associated macrophage ferroptosis and polarization.Cell death & disease · 2026Article
- Review
- Prognostic value of lymphatic vessel density in the capsule of early-stage hepatocellular carcinoma: implications for postoperative recurrence risk.Frontiers in immunology · 2026Article
- The interplay between extracellular matrix remodeling and cellular lipid metabolic reprogramming in cancer: a review.Molecular biology reports · 2025Review
- Long-chain acyl-CoA synthetases: biological functions, diseases and therapeutic targets.Molecular biomedicine · 2025Review
- Multidimensional analysis reveals the potential of ACSL3 as a cancer biomarker: from pan-cancer exploration to functional validation in hepatocellular carcinoma.Clinical and experimental medicine · 2025Article
- Bupivacaine exacerbates postoperative cognitive dysfunction by suppressing YES1-mediated YAP1 phosphorylation.Experimental brain research · 2025Article
- ACSL4 at the helm of the lipid peroxidation ship: a deep-sea exploration towards ferroptosis.Frontiers in pharmacology · 2025Review
- Novel Strategies against Hepatocellular Carcinoma through Lipid Metabolism.Oncology research · 2025Review
- Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
objectiveMitochondrial fatty acid oxidation is a metabolic pathway whose dysregulation is recognized as a critical factor in various cancers, because it sustains cancer cell survival, proliferation, and metastasis. The acyl-CoA synthetase long-chain (ACSL) family is known to activate long-chain fatty acids, yet the specific role of ACSL3 in breast cancer has not been determined.
methodsWe assessed the prognostic value of ACSL3 in breast cancer by using data from tumor samples. Gain-of-function and loss-of-function assays were also conducted to determine the roles and downstream regulatory mechanisms of ACSL3
resultsACSL3 expression was notably downregulated in breast cancer tissues compared with normal tissues, and this phenotype correlated with improved survival outcomes. Functional experiments revealed that ACSL3 knockdown in breast cancer cells promoted cell proliferation, migration, and epithelial-mesenchymal transition. Mechanistically, ACSL3 was found to inhibit β-oxidation and the formation of associated byproducts, thereby suppressing malignant behavior in breast cancer. Importantly, ACSL3 was found to interact with YES proto-oncogene 1, a member of the Src family of tyrosine kinases, and to suppress its activation through phosphorylation at Tyr419. The decrease in activated YES1 consequently inhibited YAP1 nuclear colocalization and transcriptional complex formation, and the expression of its downstream genes in breast cancer cell nuclei.
conclusionsACSL3 suppresses breast cancer progression by impeding lipid metabolism reprogramming, and inhibiting malignant behaviors through phospho-YES1 mediated inhibition of YAP1 and its downstream pathways. These findings suggest that ACSL3 may serve as a potential biomarker and target for comprehensive therapeutic strategies for breast cancer.
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