ArticleCancer science2024
ACSL4 upregulates IFI44 and IFI44L expression and promotes the proliferation and invasiveness of head and neck squamous cell carcinoma cells.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- IRF1-activated CA9 accelerates oral squamous cell carcinoma process via regulating cell glycolysis, migration, apoptosis and ferroptosis.Odontology · 2026Article
- Imaging transcriptomics in basal cell carcinoma: Coupling in vivo tumor morphology with gene expression.JID innovations : skin science from molecules to population health · 2026Article
- The ZIF-8 nanoplatform targeted delivery of IFI44 siRNA to suppress bladder cancer development via modulating the PI3K/AKT signaling pathway.Journal of nanobiotechnology · 2026Article
- Elucidating EGCG' s targets in nasopharyngeal carcinoma through combined cell-based assays and transcriptomic sequencing.Discover oncology · 2026Article
- IFI44 Promotes Clear Cell Renal Cell Carcinoma Progression via PRDX1 and Predicts Poor Prognosis.Research (Washington, D.C.) · 2026Article
- Research Progress on the Mechanisms of Traditional Chinese Medicine in Preventing and Treating HCC Invasion and Metastasis Based on Lipid Metabolic Reprogramming.Current topics in medicinal chemistry · 2026Review
- Multi-omics dissection of the genetic regulation underlying fatty acid composition in cattle.Genome biology · 2025Article
- Immune modulation following α and βOncoimmunology · 2025Article
- Single-cell RNA sequencing reveals age-related heterogeneity in the tumor microenvironment of breast cancer patients.Scientific reports · 2025Article
- TWF2 Drives Tumor Progression and Sunitinib Resistance in Renal Cell Carcinoma through Hippo Signaling Suppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Head and Neck Malignancies in Autoimmune Polyendocrine Syndrome Type 1 (APS-1/APECED): A Scoping Review of Molecular Pathogenesis, Clinical Features, and Outcomes.International journal of molecular sciences · 2025Article
- Machine learning approach to predict prognosis and immunotherapy responses in colorectal cancer patients.hLife · 2025Article
- IRF1 is a core transcriptional regulatory circuitry member promoting AML progression by regulating lipid metabolism.Experimental hematology & oncology · 2025Article
- ACSL4 upregulates IFI44 and IFI44L expression and promotes the proliferation and invasiveness of head and neck squamous cell carcinoma cells.Cancer science · 2024Article
- UnravelingFrontiers in oncology · 2024Review
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Authors and funding
7 authors.
Funding
Abstract
Reprogramming of cellular energy metabolism, including deregulated lipid metabolism, is a hallmark of head and neck squamous cell carcinoma (HNSCC). However, the underlying molecular mechanisms remain unclear. Long-chain acyl-CoA synthetase 4 (ACSL4), which catalyzes fatty acids to form fatty acyl-CoAs, is critical for synthesizing phospholipids or triglycerides. Despite the differing roles of ACSL4 in cancers, our data showed that ACSL4 was highly expressed in HNSCC tissues, positively correlating with poor survival rates in patients. Knockdown of ACSL4 in HNSCC cells led to reduced cell proliferation and invasiveness. RNA sequencing analyses identified interferon-induced protein 44 (IFI44) and interferon-induced protein 44-like (IFI44L), encoded by two interferon-stimulated genes, as potential effectors of ACSL4. Silencing IFI44 or IFI44L expression in HNSCC cells decreased cell proliferation and invasiveness. Manipulating ACSL4 expression or activity modulated the expression levels of JAK1, tyrosine kinase 2 (TYK2), signal transducer and activator of transcription 1 (STAT1), interferon α (IFNα), IFNβ, and interferon regulatory factor 1 (IRF1), which regulate IFI44 and IFI44L expression. Knockdown of IRF1 reduced the expression of JAK1, TYK2, IFNα, IFNβ, IFI44, or IFI44L and diminished cell proliferation and invasiveness. Our results suggest that ACSL4 upregulates interferon signaling, enhancing IFI44 and IFI44L expression and promoting HNSCC cell proliferation and invasiveness. Thus, ACSL4 could serve as a novel therapeutic target for HNSCC.
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