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  3. Macrophage Activation Determines Muscle Wasting In Pancreatic Cancer
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Macrophage activation determines muscle wasting in pancreatic cancer

Chia-Jung Chang1, Po-Hsien Huang2,3, Szu-Ying Chen4

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Oncogene
|May 29, 2025

View abstract on PubMed

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This summary is machine-generated.

Cachexia onset in tumor-bearing mice is linked to specific macrophage signals, particularly CHI3L1. Targeting this pathway with an anti-CHI3L1 antibody reduced muscle wasting, tumor growth, and metastasis.

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • The contribution of non-cancerous cells in the tumoral microenvironment to cachexia remains poorly understood.
  • The precise timing and cellular origins of cachexia onset are unpredictable, despite advances in cancer cachexia research.

Purpose of the Study:

  • To investigate the role of non-cancerous cells in the tumoral microenvironment in driving cachexia.
  • To identify specific cell types and molecular signals responsible for early-onset muscle wasting in a pancreatic cancer model.
  • To elucidate the CHI3L1-HDAC3 signaling axis in cachexia progression.

Main Methods:

  • Utilized a transgenic KrasLSL-G12D/+;Trp53flox/flox;Pdx1-Cre (KP2C) GEMM for pancreatic cancer.
  • Performed single-cell RNA sequencing (scRNA-seq) on peripheral blood mononuclear cells (PBMCs) and mouse-derived syngeneic transplants (MDSTs).
  • Investigated the effects of CHI3L1 on C2C12 myoblasts and utilized skeletal muscle-specific conditional Hdac3 knockout mice.

    • Main Results:

    • scRNA-seq identified CHI3L1 and CHI3L3 as differentially expressed genes, with macrophages mediating early muscle wasting.
    • Recombinant CHI3L1 suppressed myotube formation and upregulated specific inflammatory and signaling genes in myoblasts.
    • Targeting CHI3L1-HDAC3 signaling via Hdac3 knockout or anti-CHI3L1 antibody treatment reduced muscle wasting, tumor growth, and metastasis.

    Conclusions:

    • Pancreatic tumor-associated macrophages play a significant role in mediating skeletal muscle wasting.
    • The CHI3L1-HDAC3 signaling pathway is a key mechanism driving cachexia progression.
    • Targeting CHI3L1 offers a potential therapeutic strategy to combat cancer cachexia and associated tumor progression.