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Updated: Jun 17, 2026

Tumor Allotransplantation in Drosophila melanogaster with a Programmable Auto-Nanoliter Injector
05:06

Tumor Allotransplantation in Drosophila melanogaster with a Programmable Auto-Nanoliter Injector

Published on: February 2, 2021

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

Kewei Yu1, Gurpreet S Moroak1, Esther M Verheyen1

  • 1Department of Molecular Biology and Biochemistry, Centre for Cell Biology, Development and Disease, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.

Disease Models & Mechanisms
|June 16, 2026
PubMed

Insights

Cancer cachexia causes significant weight loss and has no effective treatments. This study reveals a conserved signaling pathway involving Unpaired (Upd), JAK/STAT, and Adipokinetic hormone (Akh) that drives this wasting syndrome.

Area of Science:

  • Molecular Biology
  • Genetics
  • Physiology

Background:

  • Cancer-associated cachexia is a debilitating wasting syndrome with millions of annual deaths.
  • Current therapeutic options for cachexia are limited and often ineffective.

Purpose of the Study:

  • To establish a Drosophila melanogaster model for studying cancer-associated cachexia.
  • To elucidate the molecular mechanisms underlying tumor-induced systemic wasting.

Main Methods:

  • Overexpression of Hipk and constitutively active Sik3 in Drosophila larval epithelial tissue to induce tumors.
  • Analysis of larval tissues for muscle and fat body wasting.
  • Measurement of carbohydrate levels and lipolysis.
  • Investigation of signaling pathways including JAK/STAT and the role of Unpaired (Upd) ligands, Adipokinetic hormone (Akh), and Brummer (Bmm) lipase.

Main Results:

  • The Drosophila model exhibited significant muscle and fat body wasting, increased carbohydrates, and lipolysis.
  • Tumors secreted Upd ligands, activating JAK/STAT signaling in corpora cardiaca cells.
  • This activation led to increased expression of Akh, a glucagon-like hormone.
  • Elevated Akh and the lipase Bmm were identified as key drivers of metabolic reprogramming and tissue catabolism.

Conclusions:

  • A conserved tumor-host signaling axis (Upd-JAK/STAT-Akh) was identified as a critical contributor to cancer-associated cachexia.
  • This pathway drives systemic metabolic changes and tissue wasting in the model organism.
  • The findings provide a foundation for developing novel therapeutic strategies targeting cachexia.
Keywords:
DrosophilaAkhBrummerCancer cachexiaGlucagonHipkJAK/STATOrgan wastingSik3TumorUnpaired

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