Abstract: Objective To explore the effect of S100A1 on the proliferation of human thyroid cancer SW579 cells and its mechanism. Methods The human thyroid cancer data sets GSE50901 and GSE138198 were selected, and R software was used to screen the differentially expressed genes in thyroid cancer tissues and normal thyroid tissues. The differentially expressed genes were verified with TGCA database. CCK-8 experiment was used to detect the effect of S100A1 knockdown or overexpression on the proliferation of human thyroid cancer SW579 cell. Western Blot was used to detect the effect of S100A1 on the WNT/β-catenin signaling pathway. Results A joint analysis of the data sets GSE50901 and GSE138198 showed that 97 genes were up-regulated in both data sets, and 46 genes were down-regulated. S100A1 gene is highly expressed in thyroid cancer. Knockdown of S100A1 could inhibit the proliferation of SW579 cells, and overexpression of S100A1 could promote the proliferation of SW579 cells. GSEA analysis found that WNT signal pathway was significantly enriched after knocking down S100A1 in SW579 cells, and the signal pathway activity was reduced. Western Blot results showed that the protein expression levels of β-catenin, c-myc and cyclin D1 in the siS100A1 group were significantly lower than those in the siNeg group, while the protein expression levels of β-catenin, c-myc and cyclin D1 in the S100A1 group were significant higher than those in the EGFP group. Conclusion S100A1 is highly expressed in thyroid cancer. Knockdown of S100A1 might inhibit the proliferation of thyroid cancer SW579 cells by inhibiting the activity of WNT/β-catenin signaling pathway.

Key words: S100A1, Bioinformatics, Thyroid cancer, WNT/β-catenin signaling pathway