Atti del 52° Congresso Nazionale: Società Italiana di Igiene, Medicina Preventiva e Sanità Pubblica (SItI)

Epidemiological evidence shows that individuals who maintain a lifestyle with high mobility and physical activity have a remarkably lower risk of noncommunicable diseases, with a reduction of all-cause mortality. Regarding the association between physical inactivity and cancer incidence, in a recent meta-analysis including 12 prospective cohort studies with 1.44 million participants, leisure-time physical activity in relation to risk of 26 different cancer types has been examined 1 ; the study showed that increasing levels of leisure-time physical activity was associated with lower risks of 13 of the 26 cancers investigated, regardless of body size and smoking history. Moreover, several studies suggest that exposure to exercise following the diagnosis of certain solid tumors might lower the progression of the disease and reduce cancer-related mortality 2 . These findings open to new approaches in the methodologies for cancer progression control, introducing the exercise-oncology field. Recently, Hojman and colleagues 3 reviewed the current molecular evidence about the effect of exercise on cancer. The authors describe the role of exercise in controlling cancer progression through a direct effect on tumor intrinsic factors and the interplay with whole-body exercise effects. The tumor growth-inhibitory effects could be mediated by several different mechanisms, such as the release of several systemic factors (i.e., catecholamines, myokines, etc.) and sympathetic activation, modulated during the exercise performance. The acute effect of a single exercise bouts leads to intratumoral adaptations, contributing to slower tumor progression. Moreover, growth factors such as insulin and IGFs stimulate cancer cell proliferation through the activation of their respective receptor tyrosine kinases, which trigger the major signal transduction pathways (e.g. PI3K/AKT and MAPK pathways) 4 . Chronic exercise reduces growth factor availability in the systemic milieu, and presumably in the tumor microenvironment, induced by prolonged physical inactivity 5 . Our research group is currently evaluating if the systemic response to a high-intensity endurance cycling (HIEC) test session could modulate the proliferation and the tumorigenic potential of breast or prostate cancer cells, in vitro. The study design includes the use of serum samples collected before, immediately after, and after 2 and 24 hours the exercise bouts. Serum samples were then been used in cell culture assays to evaluate cell proliferation and colony formation in a three-dimensional cell growth assay: three-dimensional anchorage-independent growth assay in soft agar is a model used to evaluate malignant cell growth and it is considered a good hallmark of tumorigenesis. In a first pilot study, blood samples of 12 healthy and sedentary females have been collected before the HIEC sessions exercise (t0, at rest), immediately after (t1), 2-hours and 24-hours post (t2 and t3, respectively) and used to supplement the culture media of cells. Our results showed that immediately-after HIEC and the 2-hours post (t1 and t2) sera markedly reduced cell proliferation capacity of triple-negative breast cancer cells (TNBC), in comparison to that revealed in cells cultured with t0 sera. Moreover, the capacity of post-exercise-conditioned sera to induce tumorigenesis in soft agar was significantly lower in comparison to that revealed in cells cultured with t0 sera.