EGFR may participate in immune evasion through regulation of B7‑H5 expression in non‑small cell lung carcinoma

作者：Zhaohui Dong, Lanying Zhang, Wei Xu, Gensheng Zhang · 发表于：Molecular Medicine Reports · 年份：2018 · DOI：10.3892/mmr.2018.9361 · 被引用次数：14 · 研究领域：Cancer Immunotherapy and Biomarkers、Cytokine Signaling Pathways and Interactions、Melanoma and MAPK Pathways

Lung cancer is one of the most prevalent malignancies worldwide; it has been ranked the most lethal type of cancer. Non‑small cell lung carcinoma (NSCLC) comprises >80% of all types of lung cancer. Although certain achievements have been made in the treatment of NSCLC, including the targeted gene drug epidermal growth factor receptor‑tyrosine kinase inhibitor (EGFR‑TKI), the five‑year survival rate of patients has not significantly increased. A previous study demonstrated that B7‑H5, a novel co‑stimulatory molecule in the B7 molecule family, was negatively correlated with EGFR in pancreatic cancer. Thus, in the present study, we aimed to investigate whether EGFR participates in immune evasion, probably through regulation of B7‑H5 expression. NCI‑H1299 NSCLCL cells were divided into control, mock, small interfering‑EGFR and EGFR‑TKI groups. The cell viability and apoptosis rate were analysed by a Cell Counting Kit‑8 assay and flow cytometry. The transforming growth factor (TGF)‑β and interleukin (IL)‑10 content was measured using an ELISA. The expression levels of EGFR, B7‑H5, Survivin, apoptosis regulator Bax, apoptosis regulator Bcl‑2 (Bcl‑2), TGF‑β, vascular endothelial growth factor (VEGF), IL‑10 and cyclooxygenase (COX)‑2 were assessed via quantitative PCR and western blotting. The activation of the tyrosine‑protein kinase JAK2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signalling pathway was detected using western blotting. The results demonstrated...