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Drug Res (Stuttg) 2015; 65(2): 70-73
DOI: 10.1055/s-0034-1372614
Original Article
© Georg Thieme Verlag KG Stuttgart · New York

Expression of HPV-16 E6 Protein and p53 Inactivation Increases the Uterine Cervical Cancer Invasion

X. Yang   *
1   Fifth Affiliated Hospital of Xinjiang Medical University, Urumqi, P.R. China
,
L. Lu   *
2   Urumqi MCH, Urumqi, P.R. China
› Author Affiliations
Further Information

Publication History

received 09 March 2014

accepted 20 March 2014

Publication Date:
15 May 2014 (online)

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Abstract

Introduction:

Human papillomavirus infection (HPV-16) and expression of HPV E6 protein are the major risk factors of cervical cancer. Studies reported that expression of E6 protein adversely affect the function of p53 and thus involved in tumor progression. In the present study, we made an attempt to analyze the prevalence of HPV-16 association, E6 and p53 expression in cervical cancer tissues.

Methods:

Uterine cervical cancer (n=10) and corresponding normal epithelium tissues (n=10) were collected at the time of surgery. The HPV-16 integration and E6 expression were analyzed by PCR and immunohistostaining. Further, p53 and Ki67 expression were analyzed by immunohistostaining. Telomerase was detected using a modified TRAP (telomerase repeat amplification protocol) assay.

Results:

We have found that almost 90% of the collected cervical cancer DNA samples showed positivity to HPV-16 and more than 60% of DNA samples were E6 positive. Further, these tissues were highly positive to p53 and Ki67 protein which contribute to apoptosis resistance and increased cell proliferation. We also found elevated level of telomerase expression in cancer tissues compared to control.

Conclusions:

The association of HPV infection and E6 expression increases the risk of cervical cancer. Further, E6 expression is the cause for inactivation of p53 in tumor tissues and deregulated cell proliferation and thus favors for tumor invasion.

Key words

cervix - human papillomavirus - cell proliferation - apoptosis - tumor progression

* These authors contributed equally to this work.


 

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