AI Article Synopsis

  • PD-L1 expression's ability to predict the effectiveness of EGFR-TKIs in NSCLC is debated, with recent studies suggesting various pathways can influence its signaling.
  • Researchers investigated how mechanisms like STAT3, AKT, and BIM expression impact PD-L1's prognostic significance in EGFR mutant advanced NSCLC patients who received treatment.
  • Results showed that high BIM expression correlated with shorter progression-free survival, indicating that BIM may be a crucial factor in determining the response to EGFR-TKIs like gefitinib, highlighting a need for further studies to confirm these findings.

Article Abstract

The role of Programmed Cell Death Ligand 1 (PD-L1) expression in predicting epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) efficacy remains controversial. Recent studies have highlighted that tumor-intrinsic PD-L1 signaling can be modulated by STAT3, AKT, MET oncogenic pathway, epithelial-mesenchymal transition, or BIM expression. This study aimed to investigate whether these underlying mechanisms affect the prognostic role of PD-L1. We retrospectively enrolled patients with EGFR mutant advanced stage NSCLC who received first-line EGFR-TKI between January 2017 and June 2019, the treatment efficacy of EGFR-TKI was assessed. Kaplan-Meier analysis of progression-free survival (PFS) revealed that patients with high BIM expression had shorter PFS, regardless of PD-L1 expression. This result was also supported by the COX proportional hazard regression analysis. In vitro, we further proved that the knockdown of BIM, instead of PDL1, induced more cell apoptosis following gefitinib treatment. Our data suggest that among the pathways affecting tumor-intrinsic PD-L1 signaling, BIM is potentially the underlying mechanism that affects the role of PD-L1 expression in predicting response to EGFR TKI and mediates cell apoptosis under treatment with gefitinib in EGFR-mutant NSCLC. Further prospective studies are required to validate these results.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9998621PMC
http://dx.doi.org/10.1038/s41598-023-30565-4DOI Listing

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