ArticleCancer cell international2024
ACADL-YAP axis activity in non-small cell lung cancer carcinogenicity.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- 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
- Multi-omic data integration and exploiting metabolic models using systems biology approach increase precision in subtyping and early diagnosis of cancer.Quantitative biology (Beijing, China) · 2025Article
- Identification of DNA damage response and crotonylation-related biomarkers for lung adenocarcinoma via machine learning and WGCNA.Clinical and experimental medicine · 2025Article
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11 authors at 4 institutions in 1 country.
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Abstract
backgroundThe role of Acyl-CoA dehydrogenase long chain (ACADL) in different tumor types had different inhibiting or promoting effect. However, its role in non-small cell lung cancer (NSCLC) carcinogenicity is not clear.
methodIn this study, we utilized The Cancer Genome Atlas (TCGA) database to analyze ACADL expression in NSCLC and its correlation with overall survival. Furthermore, we investigated the function of ACADL on cellular proliferation, invasion, colony, apoptosis, cell cycle in vitro with NSCLC cells. Mechanistically, we evaluated the regulatory effect of ACADL expression on its downstream factor yes-associated protein (YAP) by assessing YAP phosphorylation levels and its cellular localization. Finally, we verified the tumorigenic effect of ACADL on NSCLC cells through xenograft experiments in vivo.
resultsCompared to adjacent non-cancerous samples, ACADL significantly down-regulated in NSCLC. Overexpression of ACADL, effectively reduced the proliferative, colony, and invasive capabilities of NSCLC cells, while promoting apoptosis and inducing cell cycle arrest. Moreover, ACADL overexpression significantly enhanced YAP phosphorylation and hindered its nuclear translocation. However, the inhibitory effect of the overexpression of ACADL in NSCLC cells mentioned above can be partially counteracted by YAP activator XMU-MP-1 application both in vitro and in vivo.
conclusionThe findings suggest that ACADL overexpression could suppress NSCLC development by modulating YAP phosphorylation and limiting its nuclear shift. This role of ACADL-YAP axis provided novel insights into NSCLC carcinogenicity and potential therapeutic strategies.
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