ArticleMedical oncology (Northwood, London, England)2023
ACADL suppresses PD-L1 expression to prevent cancer immune evasion by targeting Hippo/YAP signaling in lung adenocarcinoma.
Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- Integrative Bulk and Single-Cell Transcriptomic Analysis Identifies a Hypoxia- and Lipid Metabolism-Related Prognostic Signature in Oral Squamous Cell Carcinoma: A Retrospective Study.International journal of molecular sciences · 2026Article
- Fatty acid metabolic reprogramming in the tumor microenvironment: Unraveling mechanisms and therapeutic prospects.Genes & diseases · 2026Review
- Multi-omics mapping identifies CYBA-mediated mitochondrial dysfunction driving macrophage polarization and ferroptosis via Nrf2 pathway in atherosclerosis.APL bioengineering · 2026Article
- Integrated transcriptomic analysis and experimental validation identify ACADL as a mitochondrial tumor suppressor via the FOXO3a/PUMA axis in lung adenocarcinoma.European journal of medical research · 2026Article
- Research progress on glioma drug resistance: mechanism analysis and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Prognostic value of fatty acid metabolism-related genes in colorectal cancer.International journal of clinical and experimental pathology · 2026Article
- SLPI⁺ AT2-Like Cells Orchestrate Lung Adenocarcinoma Invasion via Wnt Pathway Activation and Stromal Crosstalk in a Spatially Defined Margin Niche.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MISP promotes the progression of lung adenocarcinoma through Inhibition of the Hippo signaling pathway.Discover oncology · 2025Article
- Effect of Transferrin-Modified FeThoracic cancer · 2025Article
- Mitochondrial cholesterol metabolism related gene model predicts prognosis and treatment response in hepatocellular carcinoma.Translational cancer research · 2024Article
- Structural basis for expanded substrate specificities of human long chain acyl-CoA dehydrogenase and related acyl-CoA dehydrogenases.Scientific reports · 2024Article
- Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine.The EPMA journal · 2024Review
- Structural Basis for Expanded Substrate SpeciResearch square · 2024Article
- ACADL-YAP axis activity in non-small cell lung cancer carcinogenicity.Cancer cell international · 2024Article
- The impact of different levels of wheat diets on hepatic oxidative stress, immune response, and lipid metabolism in Tibetan sheep (Ovis aries).BMC veterinary research · 2024Article
- YAP at the Crossroads of Biomechanics and Drug Resistance in Human Cancer.International journal of molecular sciences · 2023Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Lung cancer is the leading cause of cancer-related death. Cancer immune evasion is a key barrier in the treatment of lung cancer and the development of effective anticancer therapeutics. Long-chain Acyl-CoA dehydrogenase (ACADL), a key enzyme that regulates β-oxidation of long-chain fatty acyl-CoAs, has been found to act as a tumor suppressor in cancers. However, the role of ACADL in lung adenocarcinoma (LUAD) has not been explored. In the current study, we find that ACADL functions as a tumor suppressor in LUAD to inhibit proliferation and enhanced chemotherapeutic drug-induced apoptosis. Interestingly, ACADL prevents tumor immune evasion by suppressing PD-L1 expression in LUAD. ACADL is critical for Hippo/YAP pathway-mediated PD-L1 regulation. Moreover, YAP activation is essential for ACADL suppression of PD-L1 transcription. In addition, ACADL increases the protein stability and kinase activity of LATS kinase to inhibit YAP activation and PD-L1 transcription. Furthermore, we show that ACADL expression is positively correlated with a better OS and FP in LUAD. Our data reveals that ACADL could be a promising target for regulating Hippo/YAP pathway to prevent tumor immune evasion in LUAD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.