ArticleTranslational lung cancer research2025
Targeting of arachidonic acid-modulated autophagy to enhance the sensitivity of
Article in Translational lung cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Targeting arachidonic acid-modulated autophagy: a novel axis in crizotinib resistance.Translational lung cancer research · 2025Article
- Arachidonic acid-mediated autophagy regulation drives crizotinib resistance in lung cancer: therapeutic opportunities and challenges.Translational lung cancer research · 2025Article
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15 authors.
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Abstract
Background: As an approved targeting drug, crizotinib has been widely used in the treatment of patients with non-small cell lung cancer (NSCLC) with anaplastic lymphoma kinase ( Methods: We first established a model for crizotinib resistance in HCC78 and H3122 cells. Next, the level of proliferation, apoptosis, autophagy flux, and reactive oxygen species (ROS) of these cells were measured. Subsequently, we analyzed the published single-cell RNA sequencing data from three Results: Crizotinib induced cell apoptosis and growth arrest by promoting the accumulation of autophagosomes through the inhibition of autophagy flux in Conclusions: We discovered a new mechanism of first generation ALK- and ROS1-TKIs resistance, which points to the role of the metabolite AA in resistance to tyrosine kinase inhibitors. It may potentially provide an alternative strategy to overcoming crizotinib resistance in NSCLC treatment by reversing AA-mediated autophagy.
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