PELI3-Mediating Epithelial-Mesenchymal Transition Correlates with Radiation Sensitivity in Non-Small Cell Lung Cancer

Radiotherapy remains a cornerstone of treatment for non-small cell lung cancer (NSCLC). Despite its critical role, the emergence of radiation resistance remains a significant hurdle, often leading to therapeutic failure and disease progression. This research aimed to investigate the expression of Pellino E3 ubiquitin protein ligase family member 3 (PELI3) in NSCLC and examine its involvement in modulating the tumor's response to radiation.

To quantify PELI3 levels in NSCLC tissues, real-time PCR and Western blotting techniques were employed. The effects of silencing PELI3 on cancer cell proliferation were evaluated using CCK-8 and colony formation assays. Furthermore, an in vivo mouse xenograft model was used to corroborate the in vitro results.

PELI3 expression was markedly elevated in NSCLC tumor samples relative to normal tissues and showed a strong association with clinical features, such as tumor volume, lymph node involvement, and radiotherapy responsiveness. Further analysis revealed that PELI3 promoted epithelial-to-mesenchymal transition (EMT) following radiation exposure. Suppressing PELI3 expression mitigated radiation-induced EMT in both cellular and animal models.

Elevated PELI3 promotes radiation-induced EMT and radioresistance in NSCLC. Suppressing PELI3 reverses EMT features and enhances radiosensitivity in vitro and in vivo, highlighting PELI3 as a potential biomarker and therapeutic target to improve radiotherapy outcomes.

These findings suggest that PELI3 could serve as a valuable prognostic marker in NSCLC and may represent a promising target to improve tumor sensitivity to radiotherapy.