Abstract
The mechanisms by which retinoblastoma 1 (RB1) mediates oncosuppressive functions are still being elucidated. We found that radiation-induced senescence in the bone depends on RB1 and is associated with the secretion of multiple bioactive factors, including interleukin-6 (IL-6), as well as with the infiltration of natural killer T (NKT) cells. Importantly, the inhibition of RB1, IL-6 or NKT cells predisposed mice to radiation-induced osteosarcomas, unveiling a cancer cell-extrinsic mechanisms that underlie the oncosuppressive activity of RB1.