Premium
Inhibitors of COX activity preserve muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma
Author(s) -
Graves Erin,
Ramsay Edward,
McCarthy Donna O.
Publication year - 2006
Publication title -
research in nursing and health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.836
H-Index - 85
eISSN - 1098-240X
pISSN - 0160-6891
DOI - 10.1002/nur.20114
Subject(s) - lewis lung carcinoma , cachexia , medicine , tumor necrosis factor alpha , melanoma , skeletal muscle , wasting , catabolism , lung cancer , endocrinology , cancer , cancer research , oncology , metastasis , metabolism
Abstract Tumor‐induced skeletal muscle wasting (SMW) contributes to the fatigue and weakness experienced by persons with cancer cachexia. Tumor necrosis factor‐alpha (TNFa) and cyclooxygenase (COX) activity have been implicated in SMW in some animal models of cancer cachexia. We report that indomethacin, a nonspecific inhibitor of COX, and NS398, a specific inhibitor of COX2, preserved muscle mass and reduced type 1 TNF receptors in muscles of mice bearing the Lewis lung carcinoma, but not in mice bearing the B16 melanoma. These data suggest that tumor‐induced SMW can occur via a COX2‐independent pathway. The COX2‐dependent pathway may involve reducing the catabolic effects of TNFa in muscle. Further study is needed to understand the relationship between COX and SMW, and whether patients with cancer cachexia might benefit from COX inhibitors. © 2006 Wiley Periodicals, Inc. Res Nurs Health 29:87–97, 2006