Skeletal Muscle Methylome-Transcriptome Disruptions During the Onset and Progression of Colorectal Cancer-Induced Cachexia

Cancer cachexia (CC) is experienced by 80% of cancer patients, representing up to 40% of cancer-related deaths. Evidence suggests biological sex dimorphism associated with CC. The initial triggering factors of muscle wasting, biological sex differences, and the epigenetic regulation during the onset and progression of cancer cachexia are not fully understood. The purpose of this study was to define the time course of C26-induced CC in males and females using transcriptomics, compare the transcriptomic changes with a more sever APC+/Min genetic model and identify the impact of epigenetic regulations (methylation) associated to CC. Overall design: At week-old Balb/c male and female mice (n=6-8/group) receivd 1x10^6 C26 cells injected bilateral, and tumors were developed for 10-, 20-, and 25-days, at endpoints, Tibialis Anterior (TA) muscle were collected. The control mice received PBS injections and TAs were colllected 25-days after PBS injections (controls). TA was also collected from 20-weeks-old APC+/Min mice (C57 black mice background) and their wild types (controls). DNA was extracted for RRBS.