Inhibitors of COX Activity Preserve Muscle Mass in Mice Bearing the Lewis Lung Carcinoma, But Not the B16 Melanoma

Document Type

Article

Language

eng

Format of Original

11 p.

Publication Date

4-2006

Publisher

Wiley

Source Publication

Research in Nursing and Health

Source ISSN

0160-6891

Original Item ID

doi: 10.1002/nur.20114; Shelves: RT1 .R48x Raynor Memorial Periodicals

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

Comments

Research in Nursing and Health, Vol. 29, No. 2 (April 2006): 87-97. DOI.

Donna McCarthy was affiliated with the National Institute of Nursing Research at the time of publication.

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