ArticlePLoS genetics2013
Myc-driven overgrowth requires unfolded protein response-mediated induction of autophagy and antioxidant responses in Drosophila melanogaster.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 92 citations in OpenAlex.
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- A Very-low-energy Fast Involves Increased Adipose Inflammatory Gene Expression: A 6-day Feeding Trial (FASTOMICS-6).The Journal of clinical endocrinology and metabolism · 2026Article
- miR-137 targets Myc to regulate growth during eye development.Development (Cambridge, England) · 2025Article
- Nonautonomous Regulation of Tumor Growth.Advances in experimental medicine and biology · 2025Review
- Article
- Interplay between autophagy and CncC regulates dendrite pruning inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Maintenance of proteostasis by Drosophila Rer1 is essential for competitive cell survival and Myc-driven overgrowth.PLoS genetics · 2024Article
- Review
- Article
- Growth deregulation and interaction with host hemocytes contribute to tumor progression in a Drosophila brain tumor model.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Disagreement among the three musketeers of the unfolded protein response.The Journal of cell biology · 2023Article
- PERK prevents rhodopsin degradation during retinitis pigmentosa by inhibiting IRE1-induced autophagy.The Journal of cell biology · 2023Article
- HTT (huntingtin) and RAB7 co-migrate retrogradely on a signaling LAMP1-containing late endosome during axonal injury.Autophagy · 2023Article
- Ubiquitylation of unphosphorylated c-myc by novel E3 ligase SCFCancer biology & therapy · 2022Article
- MYC and therapy resistance in cancer: risks and opportunities.Molecular oncology · 2022Review
- Paradoxical effects of DNA tumor virus oncogenes on epithelium-derived tumor cell fate during tumor progression and chemotherapy response.Signal transduction and targeted therapy · 2021Article
- Expression of Human Mutant Preproinsulins Induced Unfolded Protein Response,International journal of molecular sciences · 2021Article
- Rationale for MYC imaging and targeting in pancreatic cancer.EJNMMI research · 2021Review
- Inhibition of autophagy rescues muscle atrophy in a LGMDD2 Drosophila model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
5 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 1 country.
Funding
Abstract
Autophagy, a lysosomal self-degradation and recycling pathway, plays dual roles in tumorigenesis. Autophagy deficiency predisposes to cancer, at least in part, through accumulation of the selective autophagy cargo p62, leading to activation of antioxidant responses and tumor formation. While cell growth and autophagy are inversely regulated in most cells, elevated levels of autophagy are observed in many established tumors, presumably mediating survival of cancer cells. Still, the relationship of autophagy and oncogenic signaling is poorly characterized. Here we show that the evolutionarily conserved transcription factor Myc (dm), a proto-oncogene involved in cell growth and proliferation, is also a physiological regulator of autophagy in Drosophila melanogaster. Loss of Myc activity in null mutants or in somatic clones of cells inhibits autophagy. Forced expression of Myc results in cell-autonomous increases in cell growth, autophagy induction, and p62 (Ref2P)-mediated activation of Nrf2 (cnc), a transcription factor promoting antioxidant responses. Mechanistically, Myc overexpression increases unfolded protein response (UPR), which leads to PERK-dependent autophagy induction and may be responsible for p62 accumulation. Genetic or pharmacological inhibition of UPR, autophagy or p62/Nrf2 signaling prevents Myc-induced overgrowth, while these pathways are dispensable for proper growth of control cells. In addition, we show that the autophagy and antioxidant pathways are required in parallel for excess cell growth driven by Myc. Deregulated expression of Myc drives tumor progression in most human cancers, and UPR and autophagy have been implicated in the survival of Myc-dependent cancer cells. Our data obtained in a complete animal show that UPR, autophagy and p62/Nrf2 signaling are required for Myc-dependent cell growth. These novel results give additional support for finding future approaches to specifically inhibit the growth of cancer cells addicted to oncogenic Myc.
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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.