ArticleCancer cell international2026
PDPK1 activates BIRC3 via NFKB1 to promote radiotherapy resistance in lung adenocarcinoma.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Radiotherapy resistance (RT resistance) remains a major obstacle in lung adenocarcinoma (LUAD) treatment, with dysregulated apoptosis being a key contributor. This study aim to investigate the role of PDPK1 in RT resistance in LUAD and its molecular mechanism. RT-resistant sublines (A549R/PC9R) were established via fractionated irradiation. Bioinformatic analysis (GSE197236 dataset) was performed to identify differentially expressed genes (DEGs). RNA sequencing, qPCR, ChIP, and dual-luciferase assays were conducted to elucidate the underlying mechanism. Cell viability, colony formation, and apoptosis were performed to functional validation. Results showed that PDPK1 was significantly upregulated in RT-resistant cells. PDPK1 knockdown inhibited cell viability and colony formation while promoting apoptosis in A549R and PC9R cells. Mechanistically, PDPK1 activated NFKB1, which in turn transactivated BIRC3, a key anti-apoptotic protein. BIRC3 overexpression reversed the pro-apoptotic effects of PDPK1 knockdown, restoring cell survival. These findings establish the PDPK1/NFKB1/BIRC3 signaling axis as a critical driver of RT resistance in NSCLC. In conclusion, our study reveals a novel molecular mechanism by which PDPK1 mediates RT resistance through the NFKB1/BIRC3 axis. Targeting this signaling pathway may represent a promising strategy to overcome RT resistance in LUAD.
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