Expression of p27,cyclin E and human papillomavirus virus(HPV) 16 proteins in human cervix carcinoma and their relationship with prognosis

Objective:To investigate the effects of inhibitor cell cycle regulation-p27,cyclin E and HPV 16 proteins in the genesis and progression of human cervix carcinoma and their clinicopathological and prognostic significance.Methods:To investigate the expressions of p27,cyclin E and HPV 16 proteins by Poly-HRP immunohistochemical technique in tumor tissues of 48 patients with invasive cervix carcinoma(ICC) and 13 cases with cervical intraepithelial neoplasia(CIN) and 15 cases with normal cervical epithelium..Results:p27 protein positive-expression rate in ICC was 25.00%,which was lower than those in normal cervical epithelial and CIN tissues(χ~(2)=29.253,P0.01),p27 protein positive-expression correlated significantly with tumor cell differentiation(χ~(2)=7.704,P0..01).Cyclin E positive-expression rate in tumor tissues was 77.08%,which was higher than that in normal cervical epithelial tissues(χ~(2)=19.695,P0.01),and there was no significant difference in cyclin E staining between ICC and CIN groups(P0.05)..Cyclin E positive-expression rate also correlated significantly with tumor cell differentiation and lymph node metastasis(χ~(2)=9.148,P0.01;χ~(2)=4.737,P0..05).HPV 16 protein positive-expression rate was 70.83% in ICC,which was higher than that in normal cervical epithelial tissues(χ~(2)=12.184,P0.01),and there was no significant difference in HPV 16 staining between ICC and CIN groups(P0.05),there was significant negative correlation between p27 protein positive-expression and cyclin E and HPV 16 positive-expression((r=-0.563),P0.01;r=-0.587,P0.01),and cyclin E positive-expression correlated significantly with HPV 16 protein positive-expression((r=0.566),P0.01).Conclusion:The decreased expression or loss of p27 protein and/or over-expression of cyclin E protein may play an important role in the genesis and progression of cervix carcinoma,HPV 16 may induce immortalization of cell and result in cervical carcinogenesis through activation of cyclin E and down-regulation of p27.