The indicative function of Twist2 and E-cadherin in HPV oncogene-induced epithelial-mesenchymal transition of cervical cancer cells.

High-risk human papillomavirus (HR-HPV) infections are among the most important factors for cervical carcinogenesis. However, whether patients infected with HR-HPV eventually develop a malignant tumor, largely depends on epithelial-mesenchymal transition (EMT), which plays an extraordinary role in the process of carcinogenesis and metastasis. Therefore, we evaluated the protein levels of EMT-related genes in normal cervical squamous epithelium, cervical intraepithelial neoplasia (CIN), and cervical squamous cell carcinoma (SCC) by tissue microarray and immunohistochemical staining. By comparing the expression of EMT-related proteins in 31 cases of cervical tumors and tumor adjacent tissues and exploring the relationship between HPV16 oncogenes and EMT in vitro, we found that Twist2 protein levels were significantly higher in CIN and cervical cancer than in normal cervical squamous epithelial samples (p<0.01 and p<0.001, respectively). This finding corresponded with the decreased expression of E-cadherin in cervical cancer. The difference in the expression of Twist2 and E-cadherin between 31 cases of cervical tumors and tumor adjacent tissues was statistically significant (p<0.01). HPV16 oncogenes were able to induce morphological alterations in the SiHa cell line, upregulate the expression of Twist2 and vimentin, downregulate E-cadherin in vitro, and exert an effect on invasion. Thus, joint detection of Twist2 and E-cadherin expression can help evaluate and provide greater insight into cervical carcinogenesis and progression.