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Updated: Jun 15, 2026
Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Mechanistic characterization of a Drosophila model of paraneoplastic nephrotic syndrome
Jun Xu1,2, Ying Liu3, Fangying Yang4
1CAS Key Laboratory of Insect Developmental and Evolutionary Biology, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai, China. junxu@cemps.ac.cn.
Abstract:
Paraneoplastic syndromes occur in cancer patients and originate from dysfunction of organs at a distance from the tumor or its metastasis. A wide range of organs can be affected in paraneoplastic syndromes; however, the pathological mechanisms by which tumors influence host organs are poorly understood. Recent studies in the fly uncovered that tumor secreted factors target host organs, leading to pathological effects. In this study, using a Drosophila gut tumor model, we characterize a mechanism of tumor-induced kidney dysfunction. Specifically, we find that Pvf1, a PDGF/VEGF signaling ligand, secreted by gut tumors activates the PvR/JNK/Jra signaling pathway in the principal cells of the kidney, leading to mis-expression of renal genes and paraneoplastic renal syndrome-like phenotypes. Our study describes an important mechanism by which gut tumors perturb the function of the kidney, which might be of clinical relevance for the treatment of paraneoplastic syndromes.
Insights
Gut tumors can cause distant kidney problems by secreting Pvf1, a signaling ligand. This activates a pathway in kidney cells, leading to paraneoplastic renal syndrome-like symptoms.
Area of Science:
- Oncology
- Nephrology
- Molecular Biology
Background:
- Paraneoplastic syndromes involve organ dysfunction distant from tumors.
- Mechanisms linking tumors to distant organ pathology are not well understood.
- Tumor-secreted factors are implicated in affecting host organs.
Purpose of the Study:
- To investigate the molecular mechanisms of tumor-induced kidney dysfunction.
- To characterize how gut tumors perturb kidney function in a Drosophila model.
Main Methods:
- Utilized a Drosophila gut tumor model.
- Analyzed the activation of the PvR/JNK/Jra signaling pathway in kidney principal cells.
- Investigated gene mis-expression in the kidney.
Main Results:
- Gut tumors secreted Pvf1, a PDGF/VEGF signaling ligand.
- Pvf1 activated the PvR/JNK/Jra pathway in kidney principal cells.
- This activation led to renal gene mis-expression and paraneoplastic renal syndrome-like phenotypes.
Conclusions:
- Discovered a mechanism where gut tumors induce kidney dysfunction via Pvf1 signaling.
- This pathway activation in kidney cells contributes to paraneoplastic renal syndrome.
- Findings may offer insights into treating paraneoplastic syndromes.
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