CHEN Shaohua, ZHANG Yan, LI Ming, CI Hongfei, CAI Zhaogen, LI Nan
Objective:To investigate expressions of phosphoribosyl pyrophosphate synthetase 2(PRPS2), cyclin dependent kinase 6(CDK6), retinoblastoma(Rb) in different stages of cervical intraepithelial lesions and cervical cancer and their correlation with human papilloma virus(HPV) infection, aiming to determine the relationship of different factors with the evolution of cervical cancer and their possible regulatory mechanism. Methods: A total of 130 patients in the Department of Pathology, the First Affiliated Hospital of Bengbu Medical College from January 2018 to December 2018 were selected, including 40 cases of cervical cancer(cervical cancer group), 40 cases of high-grade squamous intraepithelial lesion(HSIL) of cervix(HSIL group), 30 cases of low-grade squamous intraepithelial lesion(LSIL) of cervix(LSIL group) and 20 cases of chronic inflammation(the control group). The expression of PRPS2, CDK6 and Rb in different grades of cervical lesions were detected using immunohistochemistry. HPV infection data of each case was collected, and the HPV infection condition and the correlation of each factor were analyzed. Results: The positive rates of PRPS2, CDK6, and Rb in the control group, LSIL group, HSIL group and cervical cancer group were (10.0%, 40.0%, 77.5%, 87.5%), (10.0%, 36.7%, 50.0%, 82.5%), and (80.0%, 63.3%, 32.5%, 10.0%) respectively, (χ2=44.02, P<0.05; χ2=31.81, P<0.05; χ2=36.08, P<0.05). There were significant differences in the expression levels of PRPS2, CDK6 and Rb between groups. The correlation analysis result indicated that protein expressions of PRPS2, CDK6 and Rb were correlated. There were differences in the HPV infection rate between groups. The expression of each factor was associated with HPV infection. Conclusion: The gradual evolution of cervical cancer was positively correlated with the overexpression of PRPS2 and CDK proteins, and related to the loss of Rb protein expression, which may accelerate transformation of cell cycle by cooperating with HPV through the CDK6-Rb-E2F pathway to promote tumor formation.