ArticleAnnals of translational medicine2022
Anlotinib suppresses lung adenocarcinoma growth via inhibiting FASN-mediated lipid metabolism.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- KLF5-driven TAZ-FASN signaling reprograms fatty acid metabolism to support Treg differentiation in lung cancer.Journal of translational medicine · 2026Article
- Anlotinib enhances the sensitivity to docetaxel in lung cancer through inhibiting DDR1-mediated glycolytic pathway.International journal of biological sciences · 2026Article
- Construction of lung adenocarcinoma subtype and prognosis model based on fatty acid metabolism-related genes.Discover oncology · 2025Article
- Elevated levels of total cholesterol and high-density lipoprotein cholesterol are associated with better prognosis in patients with lung adenocarcinoma: a retrospective cohort study.Translational cancer research · 2025Article
- The role of ESM1 in the lipids metabolic reprogramming and angiogenesis of lung adenocarcinoma cells.Heliyon · 2024Article
- Silencing of CD147 inhibits cell proliferation, migration, invasion, lipid metabolism dysregulation and promotes apoptosis in lung adenocarcinoma via blocking the Rap1 signaling pathway.Respiratory research · 2023Article
- Applying machine learning algorithms to develop a survival prediction model for lung adenocarcinoma based on genes related to fatty acid metabolism.Frontiers in pharmacology · 2023Article
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Anlotinib, a vascular endothelial growth factor receptor (VEGFR) inhibitor, has been widely used in advanced lung cancer patients, but the intrinsic mechanism of cancer cell elimination is not fully disclosed. In this study, we reported that anlotinib suppressed lung adenocarcinoma (LUAD) growth through inhibiting fatty acid synthase (FASN)-mediated lipid metabolism. Methods: To investigate the underlying mechanisms of anlotinib, an A549 cell line-derived xenograft model was constructed and a proteomics technique was employed to screen potential markers. Gas chromatography-mass spectrometry (GC-MS) profiling of medium-long chain fatty acid and neutral lipid droplet fluorescence staining were employed to detect lipid metabolism in cancer cells. Subsequently, the effects of anlotinib on FASN expression were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot. Short hairpin RNA (shRNA) knockdown of FASN was used to assess the role of FASN in the antitumor effect of anlotinib. A patient-derived xenograft (PDX) model was established to validate the efficacy of anlotinib in the patient and IHC staining of FASN was examined. Results: Our data revealed that anlotinib significantly decreased the expression of proteins related to lipid metabolism. GC-MS profiling of medium-long chain fatty acid and neutral lipid droplet fluorescence staining validated that anlotinib could disturb the fatty acid metabolism in cancer cells, especially de novo lipogenesis. Mechanically, the messenger RNA (mRNA) and protein of FASN were down-regulated by anlotinib in A549 cells and FASN knockdown could diminish the antitumor effect of anlotinib Conclusions: Anlotinib could inhibit the growth of LUAD through FASN-mediated lipid metabolism. Our findings provide new insights into the antitumor mechanism of anlotinib in lung adenocarcinoma.
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