کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1927987 | 1536771 | 2015 | 7 صفحه PDF | دانلود رایگان |
• NSCLCs with mutated EGFR express higher PD-L1 than that with wild type EGFR.
• Gefitinib, one of EGFR-TKIs, inhibits PD-L1 expression in NSCLCs.
• EGF enhances while gefitinib reduces PD-L1 in NSCLCs via NF-κB pathway.
Non-small-cell lung cancer (NSCLC) is a severe disease threatening human health. Targeted therapy of epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) has obtained potent efficacy in the treatment of NSCLC patients. However, the effects of EGFR-TKIs on tumor immune microenvironment are unclear. In this study, we show that NSCLCs with EGFR mutation express higher programmed cell death ligand 1 (PD-L1) than NSCLCs with wild type EGFR. The EGFR activation is also associated with high expression of PD-L1. The EGFR-TKI gefitinib can reduce PD-L1 expression, via inhibiting NF-κB, in EGFR mutant NSCLC in vitro and in vivo. These findings elucidate a novel anti-tumor mechanism of EGFR-TKI and provide the possibility of combined strategy of targeted therapy and immunotherapy for EGFR mutant NSCLC patients.
Journal: Biochemical and Biophysical Research Communications - Volume 463, Issues 1–2, 17–24 July 2015, Pages 95–101