ArticleDevelopmental biology2016
Wildtype adult stem cells, unlike tumor cells, are resistant to cellular damages in Drosophila.
Article in Developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- A feedback loop that drives cell death and proliferation and its defect in intestinal stem cells.Life science alliance · 2024Article
- Auxilin regulates intestinal stem cell proliferation through EGFR.Stem cell reports · 2022Article
- Phosphorylation of Yun is required for stem cell proliferation and tumorigenesis.Cell proliferation · 2022Article
- The Yun/Prohibitin complex regulates adultProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Aneuploidy facilitates dysplastic and tumorigenic phenotypes in the Drosophila gut.Biology open · 2021Article
- Metabolic reprogramming in cancer: mechanistic insights from Drosophila.Disease models & mechanisms · 2021Review
- Genomic instability and cancer: lessons fromOpen biology · 2020Review
- Tissue stem cells: the new actors in the aneuploidy field.Cell cycle (Georgetown, Tex.) · 2019Article
- Autophagy and Tumorigenesis in Drosophila.Advances in experimental medicine and biology · 2019Review
- Shavenbaby and Yorkie mediate Hippo signaling to protect adult stem cells from apoptosis.Nature communications · 2018Article
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Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Adult stem cells or residential progenitor cells are critical to maintain the structure and function of adult tissues (homeostasis) throughout the lifetime of an individual. Mis-regulation of stem cell proliferation and differentiation often leads to diseases including cancer, however, how wildtype adult stem cells and cancer cells respond to cellular damages remains unclear. We find that in the adult Drosophila midgut, intestinal stem cells (ISCs), unlike tumor intestinal cells, are resistant to various cellular damages. Tumor intestinal cells, unlike wildtype ISCs, are easily eliminated by apoptosis. Further, their proliferation is inhibited upon autophagy induction, and autophagy-mediated tumor inhibition is independent of caspase-dependent apoptosis. Interestingly, inhibition of tumorigenesis by autophagy is likely through the sequestration and degradation of mitochondria, as compromising mitochondria activity in these tumor models mimics the induction of autophagy and increasing the production of mitochondria alleviates the tumor-suppression capacity of autophagy. Together, these data demonstrate that wildtype adult stem cells and tumor cells show dramatic differences in sensitivity to cellular damages, thus providing potential therapeutic implications targeting tumorigenesis.
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Registered trials
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.