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An Iron-regulated Signalling Pathway Controls Adipose Browning and Cancer Cachexia.

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    Cancer cachexia involves white adipose tissue (WAT) browning. This study reveals that iron metabolism and methionine sulfoxide reductase A (MSRA) drive WAT browning, offering new therapeutic targets for cancer-associated metabolic disorders.

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    Area of Science:

    • Biochemistry
    • Metabolic Disorders
    • Oncology

    Background:

    • Cachexia, a lethal metabolic disorder, affects nearly half of cancer patients, characterized by white adipose tissue (WAT) browning and atrophy.
    • Pancreatic ductal adenocarcinoma (PDA) is a common cancer associated with cachexia.

    Purpose of the Study:

    • To investigate the molecular mechanisms underlying WAT browning in cancer-associated cachexia.
    • To identify key players in iron metabolism and protein oxidation involved in cachexia.

    Main Methods:

    • Utilized patient-derived specimens and pancreatic ductal adenocarcinoma (PDA) mouse models.
    • Analyzed iron metabolism and proteinaceous methionine oxidation in WAT.
    • Investigated the role of methionine sulfoxide reductase A (MSRA) and Protein Kinase A (PKA) in adipose browning.

    Main Results:

    • Identified iron influxes and proteinaceous methionine oxidation as key initiators of WAT browning.
    • Demonstrated that iron activates MSRA by promoting its multimerization and enzymatic activity.
    • Showed that MSRA maintains PKA activity by preserving methionines near its ATP-binding site.
    • MSRA deletion in PDA mouse models impaired WAT browning, mitigated cachexia, and improved survival.

    Conclusions:

    • Established the iron-MSRA-PKA axis as a critical nexus in cancer-associated cachexia.
    • This axis represents a potential therapeutic target for treating cachexia in cancer patients.