HPV-p53-miR-34a axis in HPV-associated cancers

Jiezhong Chen; Kong-Nan Zhao

doi:10.3978/j.issn.2305-5839.2015.09.39

HPV-p53-miR-34a axis in HPV-associated cancers

Ann Transl Med. 2015 Dec;3(21):331. doi: 10.3978/j.issn.2305-5839.2015.09.39.

Authors

Jiezhong Chen¹, Kong-Nan Zhao¹

Affiliation

¹ 1 School of Biomedical Sciences, The University of Queensland, St Lucia, QLD 4072, Australia ; 2 Institute of Molecular Virology and Immunology, Department of Medical Microbiology and Immunology, Wenzhou Medical University, Wenzhou 325000, China ; 3 Centre for Kidney Disease Research-Venomics Research, School of Medicine, University of Queensland, Princess Alexandra Hospital, Woolloongabba, Brisbane, QLD 4102, Australia.

PMID: 26734641
PMCID: PMC4691011
DOI: 10.3978/j.issn.2305-5839.2015.09.39

Abstract

Human papillomaviruses (HPVs) are known to cause many cancers by altering multiple signalling pathways through their oncogene integration into host genome and expression. Studies have shown that many microRNAs (miRs) may function as oncogenes (called as oncomiRs) to promote an oncogenic effect. MiR-34a among the reported oncomiRs is a key player in the carcinogenesis caused by infection with HPVs. In this mini-review, we summarise the roles of miR-34a in HPV-caused cancers. MiR-34a is transcriptionally regulated by tumour suppressor p53. HPV oncogene E6 inhibits expression of p53 to decrease the levels of miR-34a, leading to the increased expression of multiple genes which are targeted by miR-34a. The upregulation of these genes increases cancer cell proliferation, survival and migration in HPV-associated cancers.

Keywords: E6 oncogene; Notch pathway; Snail; cyclin D1; epithelial-mesenchymal transition (EMT); proliferation.

Publication types

Review