ArticleTranslational lung cancer research2025
Synergistic camrelizumab therapy inhibits P53-mutant osimertinib-resistant solid lung adenocarcinoma via the TGF-β signaling pathway.
Article in Translational lung cancer research, 2025. 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
Background: Lung adenocarcinomas (LACs) are classified into several histological types. The clinical outcomes are not consistent in epidermal growth factor receptor-tyrosine kinase inhibitor ( Methods: Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyse differentially expressed genes (DEGs) from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) (GSE68465) cohorts. Expression of PD-L1 and cytokines were analyzed by immunohistochemistry and cytometric bead array. Osimertinib-resistant solid LAC xenografts were implanted into immune-humanized mice to demonstrate pathological responses after EGFR-TKI and ICI. TGF-β signaling proteins, pERK1/2, pSTAT3, and PD-L1 was detected by western blotting. Clinical responses were observed in 12 osimertinib-resistant patients treated by ICI. Results: GO and KEGG analyses highlighted "cytokine-cytokine receptor interaction" and "TGF-beta signaling pathway". Heterogeneous PD-L1 expression was regulated by synergistic IL-6/STAT3, TGF-β and EGFR pathways. Significant tumor remission and inhibition of TGF-β signaling pathway were found in EGFR-TKI plus ICI treatment in mice models. Osimertinib-resistant solid LACs treated by ICI had better clinical outcomes. Conclusions: TGF-β signaling pathway is associated with PD-L1 expression and the pathological remission treated by EGFR-TKI and ICI. Solid osimertinib-resistant LACs by ICI can be beneficial through the inhibition of TGF-β signaling pathway.
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