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Simple Summary: Cancer continues to be a major medical challenge, highlighting the need for new treatment strategies. One promising area of research is the role of exercise-derived extracellular vesicles, which are tiny particles released from cells during physical activity. These extracellular vesicles play a key role in cell communication and can influence various cellular functions. Recent studies have shown that extracellular vesicles released during exercise contain bioactive molecules that may help combat cancer. These molecules have been found to inhibit tumor growth, prevent the spread of cancer, and improve responses to treatment. They work by modulating important signaling pathways and altering the tumor environment, which could enhance the effectiveness of cancer therapies and minimize side effects. This review aims to summarize the current understanding of how exercise-derived extracellular vesicles and their contents impact cancer biology. It will cover how these extracellular vesicles affect cancer cell behaviors like growth, proliferation, and invasion, and discuss the potential benefits and limitations of using exercise-derived extracellular vesicles as new cancer treatments. Cancer remains a major challenge in medicine, prompting exploration of innovative therapies. Recent studies suggest that exercise-derived extracellular vesicles (EVs) may offer potential anti-cancer benefits. These small, membrane-bound particles, including exosomes, carry bioactive molecules such as proteins and RNA that mediate intercellular communication. Exercise has been shown to increase EV secretion, influencing physiological processes like tissue repair, inflammation, and metabolism. Notably, preclinical studies have demonstrated that exercise-derived EVs can inhibit tumor growth, reduce metastasis, and enhance treatment response. For instance, in a study using animal models, exercise-derived EVs were shown to suppress tumor proliferation in breast and colon cancers. Another study reported that these EVs reduced metastatic potential by decreasing the migration and invasion of cancer cells. Additionally, exercise-induced EVs have been found to enhance the effectiveness of chemotherapy by sensitizing tumor cells to treatment. This review highlights the emerging role of exercise-derived circulating biomolecules, particularly EVs, in cancer biology. It discusses the mechanisms through which EVs impact cancer progression, the challenges in translating preclinical findings to clinical practice, and future research directions. Although research in this area is still limited, current findings suggest that EVs could play a crucial role in spreading molecules that promote better health in cancer patients. Understanding these EV profiles could lead to future therapies, such as exercise mimetics or targeted drugs, to treat cancer. [ABSTRACT FROM AUTHOR]

Simple Summary: Breast cancer significantly affects women globally, but physical activity (PA) has been shown to improve the quality of life, aid recovery, and enhance survival rates in patients. Studies reveal that PA influences DNA methylation, both globally and at gene-specific levels, potentially reversing abnormal methylation linked to cancer. This review compiles research on PA's impact on DNA methylation in breast cancer patients. The findings suggest that PA increases global DNA methylation in tumour tissues and alters gene-specific promoter methylation across various genes. Bioinformatic analysis indicates that these genes are primarily involved in metabolic pathways, cell cycle regulation, mitosis, cellular stress responses, and diverse binding processes. The Human Protein Atlas supports these findings, showing gene functionality in 266 tissues, including various breast tissues. Overall, PA's ability to modify DNA methylation patterns in breast cancer patients may aid in the restoration of normal cellular functions and enhance recovery and survival outcomes. Breast cancer (BC) continues to significantly impact women worldwide. Numerous studies show that physical activity (PA) significantly enhances the quality of life, aids recovery, and improves survival rates in BC patients. PA's influence extends to altering DNA methylation patterns on both a global and gene-specific scale, potentially reverting abnormal DNA methylation, associated with carcinogenesis and various pathologies. This review consolidates the findings of the current literature, highlighting PA's impact on DNA methylation in BC patients. Our systematic analysis indicates that PA may elevate global DNA methylation within tumour tissues. Furthermore, it appears to modify gene-specific promoter methylation across a wide spectrum of genes in various tissues. Through bioinformatic analysis, to investigate the functional enrichment of these affected genes, we identified a predominant enrichment in metabolic pathways, cell cycle regulation, cell cycle checkpoints, mitosis, cellular stress responses, and molecular functions governing diverse binding processes. The Human Protein Atlas corroborates this enrichment, indicating gene functionality across 266 tissues, notably within various breast tissues. This systematic review unveils PA's capacity to systematically alter DNA methylation patterns across multiple tissues, particularly in BC patients. Emphasising its influence on crucial biological processes and functions, this alteration holds potential for restoring normal cellular functionality and the cell cycle. This reversal of cancer-associated patterns could potentially enhance recovery and improve survival outcomes. [ABSTRACT FROM AUTHOR]

Biological age, reflecting the cumulative damage in the body over a lifespan, is a dynamic measure more indicative of individual health than chronological age. Accelerated aging, when biological age surpasses chronological age, is implicated in poorer clinical outcomes, especially for breast cancer (BC) survivors undergoing treatments. This preliminary study investigates the impact of a 16-week online supervised physical activity (PA) intervention on biological age in post-surgery female BC patients. Telomere length was measured using qPCR, and the ELOVL2-based epigenetic clock was assessed via DNA methylation pyrosequencing of the ELOVL2 promoter region. Telomere length remained unchanged, but the ELOVL2 epigenetic clock indicated a significant decrease in biological age in the PA group, suggesting the potential of PA interventions to reverse accelerated aging processes in BC survivors. The exercise group showed improved cardiovascular fitness, highlighting PA's health impact. Finally, the reduction in biological age, as measured by the ELOVL2 epigenetic clock, was significantly associated with improvements in cardiovascular fitness and handgrip strength, supporting improved recovery. Epigenetic clocks can potentially assess health status and recovery progress in BC patients, identifying at-risk individuals in clinical practice. This study provides potential and valuable insights into how PA benefits BC survivors' health, supporting the immediate benefits of a 16-week exercise intervention in mitigating accelerated aging. The findings could suggest a holistic approach to improving the health and recovery of post-surgery BC patients. [ABSTRACT FROM AUTHOR]