Exercise Program During Chemotherapy in Metastatic Colorectal Cancer
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Neoplasms,Stage Iv Colorectal Cancer
PROVIDER: 2241204 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:High intensity aerobic exercise (90% of the maximum heart rate) can effectively suppress cancer proliferation in vivo. However, the molecular effect of aerobic exercise and its relevance to cancer prevention remains uninvestigated. The mRNA-sequencing technique (mRNA-seq) can provide a genome-wide depiction of gene expression changes by aerobic exercise. Mice with colorectal cancer were subjected to high intensity aerobic exercise, and mRNA-seq analysis was performed on heart, lung, and skeletal muscle tissues to analyze the molecular effects of the exercise in a genome-wide manner. The skeletal muscle-derived genes with exercise-dependent differential expressions were further evaluated for their effects on colorectal cancer cell viability. Regular and high intensity aerobic physical activity in the mice produced positive results in comprehensive parameters (i.e., food intake, weight, and survival rate) compared to those in the control groups (healthy and cancer with no exercise). A heatmap of differentially expressed genes revealed markedly different expression patterns between these groups. RNA-seq analysis of 23,282 skeletal muscle-derived genes identified a number of anticancer effector genes. Knockdown and overexpression of selected anticancer genes significantly repressed CT26 proliferation by 20% (p<0.05). Our finding based on the aerobic exercise cancer mouses model suggest that the high intensity exercise resulted in a global change in gene expression patterns, particularly those that affect cancer cell viability.
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Project description:High intensity aerobic exercise (90% of the maximum heart rate) can effectively suppress cancer proliferation in vivo. However, the molecular effect of aerobic exercise and its relevance to cancer prevention remains uninvestigated. The mRNA-sequencing technique (mRNA-seq) can provide a genome-wide depiction of gene expression changes by aerobic exercise. Mice with colorectal cancer were subjected to high intensity aerobic exercise, and mRNA-seq analysis was performed on heart, lung, and skeletal muscle tissues to analyze the molecular effects of the exercise in a genome-wide manner. The skeletal muscle-derived genes with exercise-dependent differential expressions were further evaluated for their effects on colorectal cancer cell viability. Regular and high intensity aerobic physical activity in the mice produced positive results in comprehensive parameters (i.e., food intake, weight, and survival rate) compared to those in the control groups (healthy and cancer with no exercise). A heatmap of differentially expressed genes revealed markedly different expression patterns between these groups. RNA-seq analysis of 23,282 skeletal muscle-derived genes identified a number of anticancer effector genes. Knockdown and overexpression of selected anticancer genes significantly repressed CT26 proliferation by 20% (p<0.05). Our finding based on the aerobic exercise cancer mouses model suggest that the high intensity exercise resulted in a global change in gene expression patterns, particularly those that affect cancer cell viability.
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Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFM-NM-2 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Cardiac and skeletal muscle from 3 high and 3 low responder rats were examined for differential miRNA expression using Exiqon microarrays
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