REDD1 deletion attenuates cancer cachexia in mice

Authors
BA Hain, H Xu, AM VanCleave, et al

Lab
Department of Cellular and Molecular Physiology, The Penn State College of Medicine, Hershey, Pennsylvania

Journal
Journal of Applied Physiology

Abstract
Cancer cachexia is a debilitating and lethal consequence of many advanced cancers. REDD1, a negative regulator of mTORC1 activity, is an emerging target in cachexia. Our data show that skeletal muscle REDD1 expression is increased in LLC-induced cancer cachexia. Mice lacking REDD1 have attenuated skeletal muscle atrophy that is likely due to maintaining both protein synthesis and inhibiting protein degradation.

BIOSEB Instruments Used:
Grip strength test (BIO-GS3)