Abstract
Human papillomavirus (HPV) infection is a prerequisite of developing cervical cancer, approximately half of which are associated with HPV type 16. HPV 16 encodes three oncogenes, E5, E6, and E7, of which E5 is the least studied so far. Its roles in regulating replication and pathogenesis of HPV are not fully understood. Here we utilize high-throughput screening to coordinately investigate the effect of E5 on the expression of host protein-coding and microRNA genes. MicroRNAs form a class of 22nt long noncoding RNAs with regulatory activity. Among the altered cellular microRNAs we focus on the alteration in the expression of miR-146a, miR-203 and miR-324-5p and their target genes in a time interval of 96 hours of E5 induction. Our results indicate that HPV infection and subsequent transformation take place through complex regulatory patterns of gene expression in the host cells, part of which are regulated by the E5 protein.
Highlights
Human papillomavirus (HPV) infection is the major cause of cervical cancer [1] and an important etiologic agent in other anogenital cancers
At 24 hours after HPV16-E5 induction many genes involved in cell cycle were regulated
The effect of HPV16 E5 oncoprotein on the expression of cellular protein-coding genes and microRNAs in HaCaT epithelial cells was investigated in genome-wide microarray experiments
Summary
Human papillomavirus (HPV) infection is the major cause of cervical cancer [1] and an important etiologic agent in other anogenital cancers (reviewed in [2] and [3]). The E6 and E7 oncoproteins can bind to and stimulate the degradation of the tumor suppressors p53 [5,6,7] and pRb [8]. Their oncogenic potentials are largely correlated with these interactions [9,10] but their interference with the functions of other intracellular proteins plays an important role as well [11,12]. Very recently it was suggested that E5 alone might have high oncogenic potential, because E5 transgenic mice were shown to develop cervical cancer after prolonged estrogen treatment [27]. E5 potentiated the effect of E6 and E7 oncogenes in inducing cervical disease
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