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Resistance to DDP remains a significant challenge in the treatment of NSCLC. This study aimed to elucidate the mechanisms underlying DDP resistance, with a focus on the role of DNA repair pathways and cancer stem cells (CSCs) in NSCLC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>We analyzed p-DNA-PKcs expression in 60 lung cancer tissues (30 DDP-resistant and 30 DDP-sensitive tissues). Using in vitro and in vivo models, such as patient-derived organoids (PDOs) and cell line-derived xenografts, we explored the interplay between DNA repair mechanisms, CSC formation, and NF-\u03baB activation in DDP-resistant NSCLC. The therapeutic potential of targeting DNA-PKcs was also explored using the DNA-PKcs inhibitor NU7441.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Result<\/jats:title>\n                    <jats:p>Our findings revealed that p-DNA-PKcs is frequently upregulated in DDP-resistant tissues and cell lines and predicts poor prognosis. Activation of the non-homologous end joining (NHEJ) DNA repair pathway by DDP facilitated the stemness of NSCLC. Mechanistically, NF-\u03baB activation was sustained through p300-mediated acetylation of p65 in response to DNA damage, contributing to resistance against DDP. Furthermore, the combination of NU7441 with DDP significantly enhanced the anti-tumor effects in NSCLC models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study revealed that NSCLC cells acquire stemness traits through NF-\u03baB activation, with p-DNA-PKcs-induced phosphorylation of p65 being a prerequisite for p65 acetylation and sustained NF-\u03baB activation in drug-resistant cells. Targeting DNA-PKcs represents a novel and effective treatment strategy to overcome DDP resistance in NSCLC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12967-025-07282-9","type":"journal-article","created":{"date-parts":[[2025,11,21]],"date-time":"2025-11-21T15:28:45Z","timestamp":1763738925000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Cisplatin-mediated activation of NF-\u03baB promotes lung cancer stem cell formation via DNA repair pathways"],"prefix":"10.1186","volume":"23","author":[{"given":"Lingyu","family":"Zhang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiumei","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunjiang","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ShiZhong","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guibin","family":"Weng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingshui","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wansong","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,11,21]]},"reference":[{"key":"7282_CR1","doi-asserted-by":"publisher","first-page":"1477","DOI":"10.1038\/s41467-024-55068-2","volume":"16","author":"C Wang","year":"2025","unstructured":"Wang C, Li J, Chen J, Wang Z, Zhu G, Song L, et al. 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