Activin-βC modulates cachexia by repressing the ubiquitin-proteasome and autophagic degradation pathways.

ABSTRACT:

Background

Cancer-associated cachexia and muscle wasting are considered key determinants of cancer-related death and reduction in the quality of life of cancer patients. A crucial link has been established between activin signaling and skeletal muscle atrophy-hypertrophy. We previously showed that activin-βC, a novel activin-A antagonist, is a tumor modulator that abolishes the cancer-associated cachexia in a mouse genetic model of gonadal tumorigenesis, in which the normal balance of inhibin/activin signalling is disrupted by a targeted mutation in the Inha gene (inhibin α-KO mouse). This study aimed to identify the molecular mechanism by which activin-βC increases survival and abolishes cancer-associated cachexia in α-KO mice. We hypothesized that overexpression of activin-βC mod

SUBMITTER: Marino FE 

PROVIDER: S-EPMC4670746 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature