Evidence map›Paper›PMID 42299622›Full record

ArticleDisease models & mechanisms2026

A Drosophila tumor model identifies a conserved Upd-JAK/STAT-Akh signaling axis associated with metabolic changes in cancer cachexia.

Kewei Yu, Gurpreet S Moroak, Esther M Verheyen

Abstract read
In one paragraph

Article in Disease models & mechanisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Kewei YuDepartment of Molecular Biology and Biochemistry, Centre for Cell Biology, Development and Disease, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Gurpreet S MoroakDepartment of Molecular Biology and Biochemistry, Centre for Cell Biology, Development and Disease, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Esther M VerheyenDepartment of Molecular Biology and Biochemistry, Centre for Cell Biology, Development and Disease, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.ORCID 0000-0002-9795-5094

Funding

CIHR PJT-156204Natural Sciences and Engineering Research Council of Canada RGPIN/2020-06192Simon Fraser University
6 · The paper itself

Abstract

Cancer-associated cachexia is a systemic wasting syndrome with no effective therapies, and it results in millions of deaths annually. Here, we established a Drosophila model of cancer cachexia using overexpression of Hipk and constitutively active Sik3 in larval epithelial tissue. Tumor-bearing larvae had significant muscle and fat body wasting, together with elevated carbohydrates and lipolysis. Mechanistically, tumors secrete Unpaired (Upd) ligands that activate JAK/STAT signaling in corpora cardiaca cells, inducing the expression of glucagon-like hormone Adipokinetic hormone (Akh). Elevated Akh, together with the lipase Brummer (Bmm), drives this systemic metabolic reprogramming and tissue catabolism. In conclusion, this study identifies a conserved tumor-host Upd-JAK/STAT-Akh signaling axis that contributes to organ wasting.

Indexed as

CachexiaDrosophila melanogasterDrosophila ProteinsInsect HormonesJanus KinasesNeoplasmsSignal TransductionSTAT Transcription FactorsTranscription FactorsAnimalsDisease Models, AnimalLarvaLipaseBMM protein, DrosophilaDrosophila ProteinsInsect HormonesJanus KinasesLipaseSTAT Transcription FactorsTranscription FactorsAkhBrummerCancer cachexiaDrosophilaGlucagonHipkJAK/STATOrgan wastingSik3TumorUnpaired

Identifiers

PMID42299622
PMCPMC13312922

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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.