Objective: Cervical cancer ranks fourth for both incidence and mortality among females. Human papillomavirus (HPV) infection plays an important role in the pathophysiology of cervical cancer. However, the evidence that cervical cancer develops only in a small cohort of HPV-positive females suggests that additional factors may also contribute to the pathophysiology of this disease. We hypothesized that one of the possible factors is the activation of cancer stem cells (CSCs) in HPV-positive subjects. Our study aimed to evaluate the abovementioned hypothesis by determining the expression of SOX2 gene as well as the status of TP53 in HPV-positive subjects.

Patients and Methods: 150 HPV-positive subjects were recruited for assessment of: a) SOX2 gene expression by ELISA method and b) status of the TP53 gene by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).

Results: The level of SOX2 expression was elevated (7.5 ng/mL; p=0.03) in 124 (82.7%) and high (9.2 ng/mL; p=0.01) in 26 (17.3%) HPV-positive subjects, respectively. In 142 (94.7%) HPV-positive subjects, TP53 gene codon 72 polymorphisms (Pro/Pro homozygote in 102 subjects; and Arg/Pro heterozygote in 40 subjects) have been identified. Furthermore, all 26 HPV-positive subjects with high SOX2 expression level showed the TP53 codon 72 Pro/Pro homozygote polymorphism.

Conclusions: The high expression of SOX2 and failure of the regulatory function exerted by p53 tumor suppressor protein may suggest the activation of CSCs in HPV-positive subjects.