Fig. 6

Schematic diagram for the potential mechanisms by which PinX1/RBM10 interaction mediates telomerase transport to telomeres and thus regulates radiosensitivity in NSCLC. Telomere dysfunction can interfere with the properness of radiation-induced DSBs repair, resulting in extensive DNA damage. These free dsDNA fragments are trapped by DCs and activate STING-dependent activation of type I interferons, leading to radiosensitisation and immune activation. PinX1 interacts with RBM10 and assists in the localisation of telomerase to the Cajal body. Subsequently, telomerase continues to recruit to telomeres, maintains telomere stability, and inhibits activation of the cGAS-STING pathway and its mediated IR-induced anti-tumour immune effects, leading to radioresistance and immune tolerance in NSCLC