Anabolic deficits and divergent unfolded protein response underlie skeletal and cardiac muscle growth impairments in the Yoshida hepatoma tumor model of cancer cachexia.

In agreement with our previous studies in ovarian, lung, and colon cancer models (Belcher et al., 2022 ; Kim et al., 2021 , 2022 ), the Yoshida AH‐130 tumors caused a reduction in translational capacity in both skeletal and cardiac muscle, although the decline in the heart did not reach statistical significance at the time point studied.

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We also examined changes in XBP1 splicing and found a robust reduction in sXBP1 in both skeletal and cardiac muscle, although it did not achieve significance in skeletal muscle.

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