ArticlePLoS genetics2018
FoxO restricts growth and differentiation of cells with elevated TORC1 activity under nutrient restriction.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Translationally Controlled Tumor Protein (TCTP) and Growth Regulation in the Drosophila Model.Advances in experimental medicine and biology · 2025Article
- Nonautonomous Regulation of Tumor Growth.Advances in experimental medicine and biology · 2025Review
- A coherent FOXO3-SNAI2 feed-forward loop in autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- Tumour-host interactions through the lens of Drosophila.Nature reviews. Cancer · 2021Review
- Activation of matrix metalloproteinases and FoxO3a in HaCaT keratinocytes by radiofrequency electromagnetic field exposure.Scientific reports · 2021Article
- Article
- Article
- Article
- Sex-dependent and sex-independent regulatory systems of size variation in natural populations.Molecular systems biology · 2019Article
- The Hippo pathway integrates PI3K-Akt signals with mechanical and polarity cues to control tissue growth.PLoS biology · 2019Article
- Headcase and Unkempt Regulate Tissue Growth and Cell Cycle Progression in Response to Nutrient Restriction.Cell reports · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TORC1, a central regulator of cell survival, growth, and metabolism, is activated in a variety of cancers. Loss of the tumor suppressors PTEN and Tsc1/2 results in hyperactivation of TORC1. Tumors caused by the loss of PTEN, but not Tsc1/2, are often malignant and have been shown to be insensitive to nutrient restriction (NR). In Drosophila, loss of PTEN or Tsc1 results in hypertrophic overgrowth of epithelial tissues under normal nutritional conditions, and an enhanced TORC1-dependent hyperplastic overgrowth of PTEN mutant tissue under NR. Here we demonstrate that epithelial cells lacking Tsc1 or Tsc2 also acquire a growth advantage under NR. The overgrowth correlates with high TORC1 activity, and activating TORC1 downstream of Tsc1 by overexpression of Rheb is sufficient to enhance tissue growth. In contrast to cells lacking PTEN, Tsc1 mutant cells show decreased PKB activity, and the extent of Tsc1 mutant overgrowth is dependent on the loss of PKB-mediated inhibition of the transcription factor FoxO. Removal of FoxO function from Tsc1 mutant tissue induces massive hyperplasia, precocious differentiation, and morphological defects specifically under NR, demonstrating that FoxO activation is responsible for restricting overgrowth of Tsc1 mutant tissue. The activation status of FoxO may thus explain why tumors caused by the loss of Tsc1-in contrast to PTEN-rarely become malignant.
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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.