BYSTANDER EFFECT OF SENESCENT TUMOR CELLS INDUCED BY GAMMA RADIATION

SALVARREDI L.; MARRA F; PINTO L; LOPEZ L; AGUERO H; MILLAN E

San Luis

Congreso; XXXVII Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2019

Sociedad de Biología de Cuyo

Premature senescence is a cell-autonomous tumor suppression mechanism actioned by stimulus as ionizing radiation that affects cell genome integrity. However, senescence cells (SCs) secrete different factors known as senescence associated secretory phenotype (SASP) able to promote or suppress tumor growth in a non-cell-autonomous manner. In this way SASP may induce a kind of senescence in their surrounding environment cells via paracrine effects, known as bystander senescence. The aim of this study was to evaluate whether SASP from radiation induced senescent cells (RIS) induced bystander senescence in proliferating tumor cells and consequently inhibits cell proliferation. Cell cultures of murine melanoma cell line B16F0 were seeded and 24 hours later exposed or not to 10 Gy gamma radiation (iB16F0 and B16F0 cells respectively). Three days later senescence was evaluated by senescence associated β-galactosidase activity (SA- β gal). Conditioned media (CM) from B16F0 (control CM) and iB16F0 (iCM) were collected and used to evaluate the bystander effect of SASP in proliferating B16F0 cells. B16F0 cells were incubated with CMs and cell proliferation and percentage of senescence cells was measured. At three days after irradiation, a higher percentage of iB16F0 cell were found in senescence (SCs) (3 ± 2 % of B16F0 cells vs 46.9 ± 2 % of iB16F0 cells; **p