A tumor-secreted protein utilizes glucagon release to cause host wasting.

ABSTRACT: Tumor‒host interaction plays a critical role in malignant tumor-induced organ wasting across multiple species. Despite known regulation of regional wasting of individual peripheral organs by tumors, whether and how tumors utilize critical host catabolic hormone(s) to simultaneously induce systemic host wasting, is largely unknown. Using the conserved yki^3SA-tumor model in Drosophila, we discovered that tumors increase the production of adipokinetic hormone (Akh), a glucagon-like catabolic hormone, to cause systemic host wasting, including muscle dysfunction, lipid loss, hyperglycemia, and ovary atrophy. We next integrated RNAi screening and Gal4-LexA dual expression system to show that yki^3SA-gut tumors secrete Pvf1 to remotely activate its receptor Pvr in Akh-produci

SUBMITTER: Ding G 

PROVIDER: S-EPMC11808122 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature