Abstract
Cluster of differentiation 47 (CD47) serves as an important negative indicator for phagocytic cells and has been reported to be overexpressed in multiple human tumor cells. Increasing evidence has suggested that CD47 overexpression may contribute to the immune escape of tumor cells by avoiding phagocytosis. However, it is currently unclear whether CD47 participates in the tumorigenesis of thyroid cancer (TC). The aim of this study was to explore the roles of CD47 in TC. In two TC cell lines, TPC-1 and K1, the CD47 expression was determined by Western blot analysis, qRT-PCR, and flow cytometry assays. The CD47 shRNA expression vector was applied to specifically decrease CD47 expression in TPC-1 and K1 cells, and the effects of CD47 knockdown on cell proliferation, apoptosis, cycle were evaluated by flow cytometry analysis. In addition, the effects of CD47 knockdown on the expression of proteins involved in the programmed death-1 (PD-1) signaling pathway were assessed by Western blot analysis. Our results indicated that when compared with normal human thyroid follicular epithelial Nthy-ori-3-1 cells, CD47 expression was significantly upregulated in both TPC-1 and K1 cells. In the functional assay, we revealed that the knockdown of CD47 inhibited cell growth and promoted cell apoptosis. Mechanistically, the PD-L1 signaling pathway was found to be activated in TPC-1 and K1 cells, and the knockdown of CD47 significantly suppressed the activation of this pathway. In conclusion, CD47 was highly expressed in TC cells, and may serve as an oncogenic molecule to promote TC progression by regulating PD-L1 signaling.