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Mechanistic characterization of a Drosophila model of paraneoplastic nephrotic syndrome

Author

Listed:
  • Jun Xu

    (Chinese Academy of Sciences
    Blavatnik Institute, Harvard Medical School)

  • Ying Liu

    (Blavatnik Institute, Harvard Medical School)

  • Fangying Yang

    (Chinese Academy of Sciences)

  • Yurou Cao

    (Chinese Academy of Sciences)

  • Weihang Chen

    (Blavatnik Institute, Harvard Medical School)

  • Joshua Shing Shun Li

    (Blavatnik Institute, Harvard Medical School)

  • Shuai Zhang

    (Chinese Academy of Sciences)

  • Aram Comjean

    (Blavatnik Institute, Harvard Medical School)

  • Yanhui Hu

    (Blavatnik Institute, Harvard Medical School)

  • Norbert Perrimon

    (Blavatnik Institute, Harvard Medical School
    Howard Hughes Medical Institute)

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.

Suggested Citation

  • Jun Xu & Ying Liu & Fangying Yang & Yurou Cao & Weihang Chen & Joshua Shing Shun Li & Shuai Zhang & Aram Comjean & Yanhui Hu & Norbert Perrimon, 2024. "Mechanistic characterization of a Drosophila model of paraneoplastic nephrotic syndrome," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-45493-8
    DOI: 10.1038/s41467-024-45493-8
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