Literature DB >> 24504435

Physical activity and prostate gene expression in men with low-risk prostate cancer.

Mark Jesus M Magbanua1, Erin L Richman, Eduardo V Sosa, Lee W Jones, Jeff Simko, Katsuto Shinohara, Christopher M Haqq, Peter R Carroll, June M Chan.   

Abstract

PURPOSE: Vigorous physical activity after diagnosis of localized prostate cancer may reduce the risk of disease progression and prostate cancer-specific mortality. The molecular mechanisms by which physical activity may exert protective effects in the prostate remain unknown.
METHODS: We examined the associations between self-reported physical activity and gene expression patterns in morphologically normal prostate tissue of 71 men with low-risk prostate cancer on active surveillance. Differential gene expression, gene set, and pathway analyses were conducted comparing dichotomous groups defined by type, intensity, and amount of physical activity reported.
RESULTS: Cell cycling and DNA repair pathways were up-regulated in men who participated in ≥ 3 h/week vigorous activity compared with men who did not. In addition, canonical pathways involved in cell signaling and metabolism, the cellular effects of sildenafil (Viagra), and the Nrf2-mediated oxidative stress response were modulated in men who reported ≥ 3 h/week of vigorous activity. Differential expression analysis at the individual gene level revealed modest differences between men who performed vigorous activity for ≥ 3 h/week and those who did not. There were no differences in prostate gene expression in comparisons with exercise groupings that did not consider both duration and intensity of activity.
CONCLUSIONS: Prostate gene expression and pathway analyses revealed sets of transcripts that may be modulated in normal prostate tissue by participating in ≥ 3 h/week of vigorous activity after diagnosis of low-risk prostate cancer. These findings suggest potential biological mechanisms by which vigorous activity may reduce risk of prostate cancer progression and warrant further study and validation.

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Year:  2014        PMID: 24504435      PMCID: PMC3990413          DOI: 10.1007/s10552-014-0354-x

Source DB:  PubMed          Journal:  Cancer Causes Control        ISSN: 0957-5243            Impact factor:   2.506


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