Exercise is a therapeutic approach in cancer treatment, providing several benefits. Moreover, exercise is associated with a reduced risk for developing a range of cancers and for their recurrence, as well as with improving survival, even though the underlying mechanisms remain unclear. Preclinical and clinical evidence shows that the acute effects of a single exercise session can suppress the growth of various cancer cell lines in vitro. This suppression is potentially due to altered concentrations of hormones (e.g., insulin) and cytokines (e.g., tumor necrosis factor alpha and interleukin 6) after exercise. These factors, known to be involved in tumorigenesis, may explain why exercise is associated with reduced cancer incidence, recurrence, and mortality. However, the effects of short- (<8 weeks) and long-term (≥8 weeks) exercise programs on cancer cells have been reported with mixed results. Although more research is needed, it appears that interventions incorporating both exercise and diet seem to have greater inhibitory effects on cancer cell growth in both apparently healthy subjects as well as in cancer patients. Although speculative, these suppressive effects on cancer cells may be driven by changes in body weight and composition as well as by a reduction in low-grade inflammation often associated with sedentary behavior, low muscle mass, and excess fat mass in cancer patients. Taken together, such interventions could alter the systemic levels of suppressive circulating factors, leading to a less favorable environment for tumorigenesis. While regular exercise and a healthy diet may establish a more cancer-suppressive environment, each acute bout of exercise provides a further "dose" of anticancer medicine. Therefore, integrating regular exercise could potentially play a significant role in cancer management, highlighting the need for future investigations in this promising area of research.
Purpose: This study aimed to assess the influence of older vs. younger age and previous anterior cruciate ligament (ACL) injury on resting serum cartilage oligomeric matrix protein (sCOMP[tpre]) concentration, on immediate load-induced sCOMP kinetics after a 30-min treadmill walking stress (∆_sCOMP[tpost]), and on the dose-response relationship between ambulatory load magnitude and ∆_sCOMP(tpost).
Methods: A total of 85 participants were recruited in 4 groups (20-30 years: 24 healthy, 23 ACL-injured; 40-60 years: 23 healthy, 15 ACL-injured). Blood samples were collected immediately before and after a walking stress at 80%, 100%, or 120% bodyweight (BW) on 3 test days and analyzed for sCOMP concentration. Linear models were used to estimate the effect of age, knee status (unilateral ACL injury, 2-10 years prior), and sex on sCOMP(tpre), ∆_sCOMP(tpost)), and the dose-response between ambulatory load magnitude and ∆_sCOMP(tpost).
Results: We found that sCOMP(tpre) was 21% higher in older than younger participants (p < 0.001) but did not differ between ACL-injured and healthy participants (p = 0.632). Also, ∆_sCOMP(tpost) was 19% lower in older than younger participants (p = 0.030) and increased with body mass index (p < 0.001), sCOMP(tpre) (p = 0.008), and with 120%BW (p < 0.001), independent of age, ACL injury, or sex.
Conclusion: Age but not prior ACL injury influences resting sCOMP and load-induced sCOMP. The dose-response relationship between ambulatory load magnitude and load-induced sCOMP changes is not affected by age, ACL injury, or sex. A better understanding of systemic sCOMP and the role of its mechanoresponse for the understanding of osteoarthritis pathophysiology and monitoring intervention efficacy may require knowledge of individual cartilage composition and tissue-level loading parameters.
Background: Physical activity can regulate and affect gene expression in multiple tissues and cells. Recently, with the development of next-generation sequencing, a large number of RNA-sequencing (RNA-seq)-based gene expression profiles about physical activity have been shared in public resources; however, they are poorly curated and underutilized. To tackle this problem, we developed a data atlas of such data through comprehensive data collection, curation, and organization.
Methods: The data atlas, termed gene expression profiles of RNA-seq-based exercise responses (GEPREP), was built on a comprehensive collection of high-quality RNA-seq data on exercise responses. The metadata of each sample were manually curated. Data were uniformly processed and batch effects corrected. All the information was well organized in an easy-to-use website for free search, visualization, and download.
Results: GEPREP now includes 69 RNA-seq datasets of pre- and post-exercise, comprising 26 human datasets (1120 samples) and 43 mouse datasets (1006 samples). Specifically, there were 977 (87.2 %) human samples of skeletal muscle and 143 (12.8 %) human samples of blood. There were also samples across 9 mice tissues with skeletal muscle (359, 35.7 %) and brain (280, 27.8 %) accounting for the main fractions. Metadata-including subject, exercise interventions, sampling sites, and post-processing methods-are also included. The metadata and gene expression profiles are freely accessible at http://www.geprep.org.cn/.
Conclusion: GEPREP is a comprehensive data atlas of RNA-seq-based gene expression profiles responding to exercise. With its reliable annotations and user-friendly interfaces, it has the potential to deepen our understanding of exercise physiology.
Background: Regular exercise can reduce incidence and progression of breast cancer, but the mechanisms for such effects are not fully understood.
Methods: We used a variety of rodent and human experimental model systems to determine whether exercise training can reduce tumor burden in breast cancer and to identify mechanism associated with any exercise training effects on tumor burden.
Results: We show that voluntary wheel running slows tumor development in the mammary specific polyomavirus middle T antigen overexpression (MMTV-PyMT) mouse model of breast cancer but only when mice are not housed alone. We identify the proteoglycan decorin as a contraction-induced secretory factor that systemically increases in patients with breast cancer immediately following exercise. Moreover, high expression of decorin in tumors is associated with improved prognosis in patients, while treatment of breast cancer cells in vitro with decorin reduces cell proliferation. Notwithstanding, when we overexpressed decorin in murine muscle or injected recombinant decorin systemically into mouse models of breast cancer, elevated plasma decorin concentrations did not result in higher tumor decorin levels and tumor burden was not improved.
Conclusion: Exercise training is anti-tumorigenic in a mouse model of luminal breast cancer, but the effect is abrogated by social isolation. The proteoglycan decorin is an exercise-induced secretory protein, and tumor decorin levels are positively associated with improved prognosis in patients. The hypothesis that elevated plasma decorin is a mechanism by which exercise training improves breast cancer progression in humans is not, however, supported by our pre-clinical data since elevated circulating decorin did not increase tumor decorin levels in these models.
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