Transcriptomics data on muscle atrophy in the state of cancer cachexia, as well as the therapeutic effects of Astragalus membranaceus Decoction

Cancer cachexia (CC) causes severe muscle loss in advanced cancer patients, significantly impacting their quality of life and life expectancy. The autophagy-lysosome system is a key pathway in muscle depletion in CC, yet targeted therapies are limited. This study examines how Astragalus polysaccharides (APS) from Astragalus membranaceus alleviate muscle wasting in CC mice. Mice were divided into control, model, and APS high-dose groups. Transcriptomic analysis identified differentially expressed genes (DEGs) enriched in autophagy and mitochondrial autophagy pathways. Results indicate that APS treatment normalizes the expression levels of some DEGs in cachectic muscle tissue. For instance, autophagy-related genes Gabarapl1, Ggad45b, and Igf1r return to normal levels after APS treatment. KEGG pathway analysis suggests that APS modulates the transcription of autophagy- and mitochondrial autophagy-related genes, reducing over-activated autophagy and mitochondrial autophagy activities. Collectively, our data provide additional insights into the transcriptional profiles of cachectic muscle and muscle treated with APS, highlighting the potential of APS as a therapeutic agent for mitigating muscle depletion in cancer cachexia. Overall design: Six-week-old male BALB/c nude mice were subjected to subcutaneous injection of CT-26 colon cancer cells (5×10^5 cells) into the right flank. At week 28, the entire leg muscles were dissected and homogenized, with three randomly selected samples from each group used for transcriptomic sequencing.