S100 calcium binding protein a11 (S100a11) promotes the proliferation, migration and invasion of cervical cancer cells, and activates wnt/ β-catenin signaling

Abstract

Purpose: This study is aimed to investigate the specific regulatory role of S100 calcium binding protein A11 (S100A11) on cervical cancer (CC), and reveal the potential mechanisms relating to Wnt/β-catenin signaling. Patients and methods: The expression of S100A11 in cervical squamous cell carcinoma (CSCC), adjacent non-cancerous, cervical intraepithelial neoplasia (CIN), and normal cervical tissues was detected by quantitative real-time PCR and/or immunohistochemistry. After transfection of pENTER-S100A11 or sh-S100A11-1/sh-S100A11-2, the viability, cell cycle, migration and invasion of C33A or SiHa cells were detected. The tumor volume and tumor weight were measured after injection of transfected C33A cells into mice. The expression of E-caherin (CDH2), N-caherin (CDH1), β-catenin (CTNNB1), and c-Myc (MYC) in C33A and SiHa cells was detected by Western blot. Results: The expression of S100A11 was significantly higher in CSCC tissues than in adjacent non-cancerous, CIN, and normal cervical tissues (P < 0.05). S100A11 expression was positively correlated with the FIGO stage and lymph node metastasis of CSCC patients (P < 0.05). The transfection of pENTER-S100A11 into C33A cells significantly increased the cell viability, the percentage of cells in G2/M phase, the numbers of migratory and invasive cells, as well as the tumor volume and weight in mice (P < 0.05). Overexpression of S100A11 also significantly downregulated E-caherin, and upregulated N-caherin, β-catenin, and c-Myc in C33A cells (P < 0.05). The transfection of sh-S100A11-1/sh-S100A11-2 exhibited the opposite results to that of pENTER-S100A11 on SiHa cells. Conclusion: Overexpression of S100A11 promotes the proliferation, migration, invasion, and epithelial-mesenchymal transition of CC cells, and activates Wnt/β-catenin signaling.