ArticleGlycobiology2018
Loss of heparan sulfate in the niche leads to tumor-like germ cell growth in the Drosophila testis.
Article in Glycobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- In vivo activities of heparan sulfate differentially modified by NDSTs during development.Proteoglycan research · 2024Article
- Heparan sulfate negatively regulates intestinal stem cell proliferation inBiology open · 2019Article
- Regulation of Drosophila germline stem cells.Current opinion in cell biology · 2019Review
- Establishment and characterization of Drosophila cell lines mutant for heparan sulfate modifying enzymes.Glycobiology · 2019Article
- Regulation of neuroblast proliferation by surface glia in the Drosophila larval brain.Scientific reports · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The stem cell niche normally prevents aberrant stem cell behaviors that lead to cancer formation. Recent studies suggest that some cancers are derived from endogenous populations of adult stem cells that have somehow escaped from normal control by the niche. However, the molecular mechanisms by which the niche retains stem cells locally and tightly controls their divisions are poorly understood. Here, we demonstrate that the presence of heparan sulfate (HS), a class glygosaminoglycan chains, in the Drosophila germline stem cell niche prevents tumor formation in the testis. Loss of HS in the niche, called the hub, led to gross changes in the morphology of testes as well as the formation of both somatic and germline tumors. This loss of hub HS resulted in ectopic signaling events in the Jak/Stat pathway outside the niche. This ectopic Jak/Stat signaling disrupted normal somatic cell differentiation, leading to the formation of tumors. Our finding indicates a novel non-autonomous role for niche HS in ensuring the integrity of the niche and preventing tumor formation.
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