Human papillomavirus infection induces NF-κB activation in cervical cancer: A comparison with penile cancer

Abstract

This study aimed to determine the relationship between human papillomavirus (HPV) and nuclear factor-κB (NF-κB) in cervical cancer using 62 tissues of cervical cancer, and to compare the findings to penile cancer. HPV-DNA integration is a crucial factor for malignant transformation in cervical cancer and can be identified using in situ hybridization. Of the 62 cases, HPV infection was detected in 28 (45.2%). This frequency was lower than in penile cancer (68.2%) as shown by our previous study. The earliest age of onset of cervical and penile cancer was 18 and 35, respectively, whereas the mean age of the initial diagnosis of cervical and penile cancer was 50.1 and 59.6, respectively. The discrepancies of HPV prevalence, earliest ages of onset and mean ages between cervical and penile cancer patients may result from the gender-based synergistic action of HPV associated with multiple epidemiological co-factors. Of the 28 HPV-infected cases, NF-κB expression was observed in the nucleus in 18 (64.3%), in the cytoplasm in 19 (67.9%) and in the nucleus and/or cytoplasm in 27 cases (96.4%). The overexpression of NF-κB in cervical cancer cases suggests that NF-κB activation is a key modulator in driving chronic inflammation to cancer.

Figure 1

(A) In situ hybridization for human papillomavirus signal exhibited on a section of cervical cancer. (B) In situ hybridization for human papillomavirus signal exhibited on a section of cervical cancer with a condylomatus lesion. (C) Immunohistochemical expression of NF-κB in the nucleus in cervical cancer. (D) Immunohistochemical expression of NF-κB in the cytoplasm in cervical cancer.