ArticleScientific reports2021
ALK inhibition activates LC3B-independent, protective autophagy in EML4-ALK positive lung cancer cells.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- The dual role of the crosstalk between autophagy and ferroptosis in lung cancer treatment: Advances in mechanisms and therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Knockdown of MIR205HG prevents cell proliferation, migration and invasion through autophagy and ferroptosis pathways in lung adenocarcinoma.Translational cancer research · 2025Article
- Autophagy and cancer therapy.Cancer letters · 2024Review
- Article
- Computational-Based Polyphenol Therapy for Nonsmall Cell Lung Cancer: Naringin Coamorphous Systems for Solubility and Bioavailability Enhancement.Molecular pharmaceutics · 2024Article
- Inhibition of autophagy; an opportunity for the treatment of cancer resistance.Frontiers in cell and developmental biology · 2023Review
- DSTYK inhibition increases the sensitivity of lung cancer cells to T cell-mediated cytotoxicity.The Journal of experimental medicine · 2022Article
- MgIG exerts therapeutic effects on crizotinib-induced hepatotoxicity by limiting ROS-mediated autophagy and pyroptosis.Journal of cellular and molecular medicine · 2022Article
- Article
- The Role of Phosphatidylinositol 3-Kinase Catalytic Subunit Type 3 in the Pathogenesis of Human Cancer.International journal of molecular sciences · 2021Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ALK inhibitors effectively target EML4-ALK positive non-small cell lung cancer, but their effects are hampered by treatment resistance. In the present study, we asked whether ALK inhibition affects autophagy, and whether this may influence treatment response. Whereas the impact of targeted therapies on autophagic activity previously have been assessed by surrogate marker proteins such as LC3B, we here thoroughly examined effects on functional autophagic activity, i.e. on the sequestration and degradation of autophagic cargo, in addition to autophagic markers. Interestingly, the ALK inhibitor Ceritinib decreased mTOR activity and increased GFP-WIPI1 dot formation in H3122 and H2228 EML4-ALK
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