Abstract
Background: Radioresistance poses a critical challenge to effective radiotherapy in the management of lung adenocarcinomas (LUAD). The hyperactivated PI3K-AKT pathway is one of the molecular events by which tumors become radioresistant. The AKT kinase, the downstream effector of PI3K kinase, comprised of three highly homologous isoforms, AKT1, AKT2, and AKT3. Despite several studies on AKT isoforms, the exact role of AKT3 in conferring radioresistance remains elusive.
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