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BioMed Research International
Volume 2017, Article ID 2948467, 12 pages
Research Article

HPV16 E6 Promotes Breast Cancer Proliferation via Upregulation of COX-2 Expression

1Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China
2The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, China

Correspondence should be addressed to J. Cui; moc.931@10881528731 and X. L. Qian; moc.361@30iyaijgnaw

Received 6 April 2017; Revised 10 June 2017; Accepted 3 July 2017; Published 9 November 2017

Academic Editor: Myong Cheol Lim

Copyright © 2017 Y. X. Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Breast cancer remains the leading cause of cancer-related mortality worldwide. It has been indicated that human papillomaviruses 16 (HPV16) might participate in the pathogenesis and development of breast cancer. However, the detected rate of HPV16 varies with region. We will investigate HPV16 E6 expression in North China and explore the effects and mechanism of HPV16 E6 on breast cancer proliferation in this study. Methods. The expressions of HPV16 E6 and COX-2 in paraffin-embedded tissues of the invasive ductal breast cancer were detected by qPCR and IHC. The effects of HPV16 E6 on breast cancer proliferation were determined by function studies. The mechanism of HPV16 E6 in promoting breast cancer proliferation was explored by Western blot and Dual-Luciferase Reporter Assay. Results. HPV16 E6 was positive in 28% invasive ductal breast carcinoma in North China; HPV16 E6 promoted breast cancer proliferation. Inhibition of COX-2 by siCOX-2 or Celecoxib attenuated the proliferation of breast cancer cells with HPV16 E6 expression; and the upregulation of COX-2 could be suppressed by the inhibition of NF-κB activity. Conclusion. HPV16 E6 promotes breast cancer proliferation by activation of NF-κB signaling pathway and increase of COX-2 expression. COX-2 will be a potential target for HPV16 E6-associated breast cancer.