Evaluation of calcium-binding protein A11 promotes the carcinogenesis of hypopharygeal squamous cell carcinoma via the PI3K/AKT signaling pathway.

The S100 gene family encodes low molecular weight proteins implicated in cancer progression. In the present study, we explored the effects and underlying mechanisms of calcium-binding protein A11 (S100A11 protein) in hypopharyngeal squamous cell carcinoma (HSCC). RT-qPCR and western blot analysis were used to detect the mRNA and protein expression of S100A11, EGFR, MMP2, CD44, and MMP9. CCK-8, colony formation, wound healing and transwell invasion assays were performed to evaluate the effects of S100A11 on HSCC cells. In our study, we observed that the level of S100A11 expression was significantly upregulated in HSCC tissues and cell lines. S100A11 inhibition increased the effects of 5-Fu on FaDu cells proliferation in vitro. In addition, S100A11 inhibition decreased the migration ability of FaDu cells. Additionally, the expression of migration-related proteins including EGFR, MMP2, CD44, and MMP9 were down-regulated when S100A11 was knocked down. Moreover, the expression of phosphorylated-PI3K (p-PI3K), phosphorylated-Akt (p-Akt), phosphorylated-mTOR (p-mTOR) and BCL-2 in FaDu cells were dramatically decreased. Our results suggested that S100A11 could activate the PI3K/Akt/mTOR signaling pathway in HSCC tumorigenesis.