Targeting HER3-dependent activation of nuclear AKT improves radiotherapy of non-small cell lung cancer.

ABSTRACT:

Background

AKT1 must be present and activated in the nucleus immediately after irradiation to stimulate AKT1-dependent double-strand breaks (DSB) repair through the fast non-homologous end-joining (NHEJ) repair process. We investigated the subcellular distribution of AKT1 and the role of HER family receptor members on the phosphorylation of nuclear AKT and radiation response.

Materials and methods

Using genetic approaches and pharmacological inhibitors, we investigated the subcellular distribution of AKT1 and the role of HER family receptor members on the activation of nuclear AKT in non-small cell lung cancer (NSCLC) cells in vitro. ɤH2AX foci assay was applied to investigate the role of AKT activating signaling pathway on DSB repair. A mouse tumor xenograft model was used

SUBMITTER: Toulany M 

PROVIDER: S-EPMC10083767 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature