ArticleJournal of thoracic disease2026
SMARCA4 deficiency contributes to platinum resistance in non-small cell lung cancer by activating the NF-κB-BIRC2/BIRC3 signaling axis.
Article in Journal of thoracic disease, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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10 authors.
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Abstract
Background: SMARCA4-deficient non-small cell lung cancer (NSCLC) is highly aggressive and has a limited response to conventional chemotherapy. The precise mechanisms by which SMARCA4 deficiency contributes to platinum-based chemotherapy resistance in NSCLC remain incompletely understood. This study aims to elucidate this resistance mechanism and provide a theoretical basis for precision treatment in clinical practice. Methods: The role of SMARCA4 deficiency in NSCLC was analyzed using the cBioPortal database. SMARCA4-knockdown NSCLC cell models were established. Cell proliferation was assessed using Cell Counting Kit-8 (CCK-8) and colony formation assays. Apoptosis was tested using flow cytometry. Carboplatin (CBP) sensitivity was evaluated by measuring the half maximal inhibitory concentration (IC Results: SMARCA4 deficiency correlated with a poor prognosis for NSCLC patients, and SMARCA4 knockdown promoted malignant phenotypes in NSCLC cell lines. The sensitivity to CBP treatment was attenuated by SMARCA4 downregulation, with concomitant activation of the NF-κB signaling pathway and upregulation of Conclusions: SMARCA4 deficiency contributes to platinum resistance in NSCLC by activating the NF-κB-BIRC2/BIRC3 signaling axis. Combination therapy with CBP and either an NF-κB inhibitor or an inhibitor of apoptosis proteins (IAP) inhibitor effectively reverses this resistance, providing a novel strategy for the precise treatment of SMARCA4-deficient NSCLC.
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