ArticleCell death & disease2020
Isobacachalcone induces autophagy and improves the outcome of immunogenic chemotherapy.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
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- Autophagy Modulates Immunogenic Cell Death in Cancer.Cancers · 2026Review
- The geroprotective potential of chalcones.Nature communications · 2025Review
- Recent Advances in the Synthesis and Biological Applications of Prenylated Chalcones.International journal of molecular sciences · 2025Review
- Therapeutic Implications of Ceritinib in Cholangiocarcinoma beyond ALK Expression and Mutation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Single-cell analysis of white adipose tissue reveals the tumor-promoting adipocyte subtypes.Journal of translational medicine · 2023Article
- Macrolide antibiotics activate the integrated stress response and promote tumor proliferation.Cell stress · 2023Article
- Adipose tissue macrophages: implications for obesity-associated cancer.Military Medical Research · 2023Review
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- Dietary regulation in health and disease.Signal transduction and targeted therapy · 2022Review
- Local anesthetics elicit immune-dependent anticancer effects.Journal for immunotherapy of cancer · 2022Article
- ATP and cancer immunosurveillance.The EMBO journal · 2021Review
- IGF1 receptor inhibition amplifies the effects of cancer drugs by autophagy and immune-dependent mechanisms.Journal for immunotherapy of cancer · 2021Article
- Crizotinib and ceritinib trigger immunogenic cell death via on-target effects.Oncoimmunology · 2021Article
- Caloric Restriction Mimetics in Nutrition and Clinical Trials.Frontiers in nutrition · 2021Review
- AKT as a therapeutic target for autophagy induction and cancer therapy.Oncoscience · 2021Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
A number of natural plant products have a long-standing history in both traditional and modern medical applications. Some secondary metabolites induce autophagy and mediate autophagy-dependent healthspan- and lifespan-extending effects in suitable mouse models. Here, we identified isobacachalcone (ISO) as a non-toxic inducer of autophagic flux that acts on human and mouse cells in vitro, as well as mouse organs in vivo. Mechanistically, ISO inhibits AKT as well as, downstream of AKT, the mechanistic target of rapamycin complex 1 (mTORC1), coupled to the activation of the pro-autophagic transcription factors EB (TFEB) and E3 (TFE3). Cells equipped with a constitutively active AKT mutant failed to activate autophagy. ISO also stimulated the AKT-repressible activation of all three arms of the unfolded stress response (UPR), including the PERK-dependent phosphorylation of eukaryotic initiation factor 2α (eIF2α). Knockout of TFEB and/or TFE3 blunted the UPR, while knockout of PERK or replacement of eIF2α by a non-phosphorylable mutant reduced TFEB/TFE3 activation and autophagy induced by ISO. This points to crosstalk between the UPR and autophagy. Of note, the administration of ISO to mice improved the efficacy of immunogenic anticancer chemotherapy. This effect relied on an improved T lymphocyte-dependent anticancer immune response and was lost upon constitutive AKT activation in, or deletion of the essential autophagy gene Atg5 from, the malignant cells. In conclusion, ISO is a bioavailable autophagy inducer that warrants further preclinical characterization.
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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.