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

[INTRODUCTION] 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.

[MATERIALS AND METHODS] 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.

[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.

[DISCUSSION] 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.

[CONCLUSION] 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.