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High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Heart)

ABSTRACT: High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Heart)

PROVIDER: PRJNA790844 | ENA |

REPOSITORIES: ENA

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High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Lung)

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.

2022-07-13 | GSE191284 | GEO

High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Heart)

2022-07-13 | GSE191283 | GEO

High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Gastrocnemius)

2022-07-13 | GSE191281 | GEO

High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Gastrocnemius)

Project description:High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Gastrocnemius)

| PRJNA790845 | ENA

High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Lung)

Project description:High intensity aerobic exercise suppresses cancer growth by regulating skeletal muscle-derived oncogenes and tumor suppressors (Lung)

| PRJNA790849 | ENA

Skeletal muscle gene expression changes with exercise mode, duration and intensity: STRRIDE study

Project description:Skeletal muscle adapts to exercise training of various modes, intensities and durations with a programmed gene expression response. This study dissects the independent and combined effects of exercise mode, intensity and duration to identify which exercise has the most positive effects on skeletal muscle health. Full details on exercise groups can be found in: Kraus et al Med Sci Sports Exerc. 2001 Oct;33(10):1774-84 and Bateman et al Am J Cardiol. 2011 Sep 15;108(6):838-44. This study uses a middle aged group of subjects that have 3+ markers of metabolic syndrome. One group remains an inactive control, while 5 groups undergo 9 mo supervised exercise training. Exercise groups are as follows: Inactive control (group B); Mild aerobic exercise - low amount/mod intensity (group A); Moderate aerobic exercise - low amt/vig intensity (group D); High aerobic exercise - high amt/vig intensity (group C); resistance training only (group F); and mod aerobic + resistance training (group E). Each group has 10 subjects (5 men and 5 women), however 3 subjects failed array QC, leaving 8 subjects in group E and 9 subjects in group F. Data were all analyzed pre to post training in a RM ANCOVA, covaried for age and sex or regression to determine genotype/phenotype interactions.

2015-05-14 | E-GEOD-48278 | biostudies-arrayexpress

Skeletal muscle response to high-intensity intermittent exercise training in young men

Project description:High-intensity intermittent exercise training (HIIT) has been proposed as an effective approach for improving both anaerobic and aerobic capacities. However, the molecular response of muscles to HIIT remains unknown. We used microarray to examine the effects of HIIT on global gene expression in human skeletal muscle.

2018-11-30 | GSE109657 | GEO

Role of aerobic exercise in ameliorating NASH

Project description:To investigate the effect of aerobic exercise on liver injury in nonalcoholic steatohepatitis (NASH), we established a NASH model induced by atherosclerotic (Ath) diet and intervened with aerobic exercise training.

2023-01-11 | GSE217155 | GEO

High-Intensity Aerobic Exercise Suppresses Cancer Growth by Regulating Skeletal Muscle-Derived Oncogenes and Tumor Suppressors.

Project description: Not available

| S-EPMC9254717 | biostudies-literature

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks

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 TGFβ 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.

2014-05-23 | GSE57880 | GEO

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