Mechanism of immune escape mediated by receptor tyrosine kinase KIT in thyroid cancer

Objective Thyroid cancer (TC) is one of the fastest-growing malignant tumors. This study sought to explore mechanism immune escape mediated by receptor tyrosine kinase (KIT) in TC. Methods The expression microarray TC was acquired through GEO database, and difference analysis Kyoto encyclopedia genes genomes pathway enrichment were carried out. KIT levels cell lines (K1/SW579/BCPAP) human normal thyroid cells detected using reverse transcription quantitative polymerase chain reaction western blot analysis. transfected with overexpressed (oe)-KIT CD8+ T cocultured SW579 cells. Subsequently, proliferation, migration, invasion abilities, cytokine (interferon-γ [IFN-γ]/tumor necrosis factor-α [TNF-α]) determined colony formation assay, Transwell assays, flow cytometry, enzyme-linked immunosorbent assay. phosphorylation MAPK pathway-related protein (ERK) measured After transfection oe-KIT, treated anisomycin (an activator pathway), p-ERK/ERK programmed death-ligand 1 (PD-L1) detected. Results Differentially expressed (N = 2472) obtained from database. reduced samples lower tumor than those Overexpression inhibited Specifically, abilities lowered, proliferation level elevated, IFN-γ TNF-α increased. activation downregulated PD-L1. Conclusion suppressed blocking downregulating