CKS1B regulates the radiosensitivity of lung cancer via activating the PI3K/AKT signaling pathway.

Radiotherapy is the mainstay and first-line treatment for non-small-cell lung cancer (NSCLC). However, there are no effective strategies for regulating tumor radiosensitivity. This study aimed to examine whether CDC28 protein kinase regulatory subunit 1B (CKS1B) knockdown can radiosensitize NSCLC cells. The results indicated that CKS1B overexpression promoted the proliferation, migration, and invasion of NSCLC cells following exposure to ionizing radiation (IR). In addition, A549 cell xenografts with CKS1B knockdown exhibited significantly enhanced radiosensitivity compared to wild-type xenografts. Mechanistically, it was observed that CKS1B silencing stimulated apoptosis, inhibited cell cycle progression, and weakened DNA damage repair, thereby increasing the sensitivity of NSCLC cells to IR treatment. Moreover, the CKS1B-induced radioresistance was mediated by the PI3K/AKT signaling pathway. These findings demonstrate that CKS1B influences the NSCLC treatment, suggesting that it is a potential prognostic marker for predicting the radiosensitivity of NSCLC cells.