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Tumor-Derived LIF Promotes GDF15-Driven Cachexia and Adverse Outcomes in Gastric Cancer.

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Leukemia Inhibitory Factor (LIF) drives cancer cachexia in gastric cancer by upregulating Growth Differentiation Factor 15 (GDF15), leading to muscle and fat loss. Targeting LIF signaling may offer a new therapeutic strategy for this condition.

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bile acidscancer cachexiagastric cancergrowth differentiation factor 15 (GDF15)leukemia inhibitory factor (LIF)metabolic remodelingskeletal muscle wasting

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Area of Science:

  • Oncology
  • Metabolic Syndrome
  • Molecular Biology

Background:

  • Cancer cachexia is a complex metabolic syndrome in gastric cancer, causing significant tissue loss and poor outcomes.
  • Growth Differentiation Factor 15 (GDF15) is a key mediator of cachexia, but its upstream regulation in gastric cancer is unclear.
  • Leukemia Inhibitory Factor (LIF) is implicated in tumor progression and metabolic dysregulation, suggesting a role in cachexia.

Purpose of the Study:

  • To investigate the association between LIF and GDF15 expression in gastric cancer.
  • To explore the relationship between LIF/GDF15 signaling and metabolic, inflammatory, and body composition changes.
  • To identify LIF signaling as a potential therapeutic target for gastric cancer cachexia.

Main Methods:

  • Transcriptomic profiling of gastric cancer tissues to assess LIF and GDF15 expression.
  • Correlation analysis between LIF/GDF15 levels and clinical parameters including survival, inflammation, and body composition.
  • Intratumoral bile acid profiling and experimental models to elucidate mechanisms.

Main Results:

  • LIF and GDF15 were significantly upregulated in gastric tumors, with a strong positive correlation.
  • High GDF15 expression correlated with reduced overall survival across multiple cohorts.
  • LIF/GDF15 expression linked to weight loss, inflammation, reduced serum proteins, and impaired body composition (muscle and adipose tissue).
  • Altered bile acid profiles were associated with LIF receptor activity and survival outcomes.
  • Experimental models confirmed LIF's role in promoting cancer cell proliferation and cachexia-related metabolic changes.

Conclusions:

  • The LIF/GDF15 axis is a critical driver of cancer cachexia in gastric cancer.
  • LIF signaling represents a promising therapeutic target for mitigating cachexia and improving outcomes in gastric cancer patients.