ArticleCell reports2021
Coordination of tumor growth and host wasting by tumor-derived Upd3.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 95 citations in OpenAlex.
- Macrophage restriction inScience advances · 2026Article
- Gut-derived Unpaired-3 cytokine signaling promotes systemic hypoxia tolerance in Drosophila.Disease models & mechanisms · 2026Article
- Lipid metabolism of hepatocyte-like cells supports intestinal tumor growth in Drosophila.Nature communications · 2026Article
- Article
- A Drosophila tumor model identifies a conserved Upd-JAK/STAT-Akh signaling axis associated with metabolic changes in cancer cachexia.Disease models & mechanisms · 2026Article
- Credit to the Fruit Fly: How the Tiny Insect Lights Up Our Understanding of Human Disease.Insects · 2026Review
- Tumour-driven lipid accumulation in oenocytes reflects systemic lipid alterations.PLoS genetics · 2026Article
- Renal coenzyme A (CoA) production from VB5 fuels stem cell proliferation and tumor growth.Nature communications · 2026Article
- Tumor-induced orexigenic imbalance lowers protein appetite and drives early organ wasting symptoms.Nature communications · 2026Article
- Profiling the host defense responses againstmLife · 2026Article
- Genetic dissection of signalling pathways that mediate iron-related tumor growth in a Drosophila model.PLoS genetics · 2026Article
- The Drosophila proventriculus lacks stem cells but compensates for age-related cell loss via endoreplication-mediated cell growth.Nature communications · 2026Article
- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- TF2TG: an online resource mining the potential gene targets of transcription factors in Drosophila.Genetics · 2026Article
- Xuanfei Baidu decoction alleviates intestinal inflammation and modulates microbiota distribution by suppressing IMD/NF-κB and JNK signaling pathways.Frontiers in microbiology · 2026Article
- Knockdown of PR-DUB subunit calypso in the developing Drosophila eye and wing results in mis-patterned tissues with altered size and shape.G3 (Bethesda, Md.) · 2025Article
- A JAK/STAT-Pdk1-S6K axis bypasses systemic growth restrictions to promote regeneration.Nature communications · 2025Article
- Hepatic ceramide synthesis links systemic inflammation to organelle dysfunction in cancer.bioRxiv : the preprint server for biology · 2025Article
- Adipose tissue-secreted Spz5 promotes distal tumor progression via Toll-6-mediated Hh pathway activation in Drosophila.The EMBO journal · 2025Article
- Translocation of gut bacteria promotes tumor-associated mortality by inducing immune-activated renal damage.The EMBO journal · 2025Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
yki-induced gut tumors in Drosophila are associated with host wasting, including muscle dysfunction, lipid loss, and hyperglycemia, a condition reminiscent of human cancer cachexia. We previously used this model to identify tumor-derived ligands that contribute to host wasting. To identify additional molecular networks involved in host-tumor interactions, we develop PathON, a web-based tool analyzing the major signaling pathways in Drosophila, and uncover the Upd3/Jak/Stat axis as an important modulator. We find that yki-gut tumors secrete Upd3 to promote self-overproliferation and enhance Jak/Stat signaling in host organs to cause wasting, including muscle dysfunction, lipid loss, and hyperglycemia. We further reveal that Upd3/Jak/Stat signaling in the host organs directly triggers the expression of ImpL2, an antagonistic binding protein for insulin-like peptides, to impair insulin signaling and energy balance. Altogether, our results demonstrate that yki-gut tumors produce a Jak/Stat pathway ligand, Upd3, that regulates both self-growth and host wasting.
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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.