PMC:3583298 / 4825-5613 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/3583298","sourcedb":"PMC","sourceid":"3583298","source_url":"https://www.ncbi.nlm.nih.gov/pmc/3583298","text":"Here, we show that YAP contributes to medulloblastoma growth and medulloblastoma cell survival after irradiation, through driving expression and production of Insulin-like Growth Factor 2 (IGF2) and subsequent activation of Akt. Akt activity endows tumor cells with the ability to evade the G1/S and G2/M checkpoints after irradiation, promoting their ongoing proliferation despite the presence of unrepaired DNA, thereby contributing to genomic instability. These novel findings reveal a link between oncogenic hedgehog signaling and genomic instability, and they suggest that targeting YAP- and IGF-driven signaling pathways may have therapeutic value by restoring radiosensitivity and also permitting reduction of the radiation dose required to induce medulloblastoma tumor cell death.","tracks":[]}