Abstract
High-risk human papillomavirus (HPV)-driven cancers represent a major health concern worldwide. Despite the constant effort to develop and promote vaccination against HPVs, there is still a high percentage of non-vaccinated population. Furthermore, secondary prevention programs are not ubiquitous worldwide and not widely followed. Metastatic disease is the cause of the great majority of cancer-associated deaths, making it essential to determine its underlying mechanisms and to identify actionable anti-metastatic targets. Within certain types of cancer (e.g., head and neck), HPV-positive tumors show different dissemination patterns when compared with their HPV-negative counterparts, implicating HPV-related factors in the metastatic process. Among the many groups of biomolecules dysregulated by HPV, microRNAs have recently emerged as key regulators of carcinogenesis, able to control complex processes like cancer metastization. In this review, we present recent data on the role of microRNAs in the metastization of HPV-related cancers and on their possible clinical relevance as biomarkers of metastatic disease and/or as therapeutic targets.
Highlights
High-risk human papillomavirus (HPV) infection occurs at the basal cell layer of the stratified squamous epithelium and these viruses are established carcinogens of the cervix, head and neck, anus, penis, vagina and vulva [1]
This review focuses on the role of miRNAs in the biology of the metastatic process and their clinical usefulness in cancers associated with HPV
In silico analysis demonstrated that miR-106b-5p promotes the progression of cervical cancer by modulating the expression of glycogen synthase kinase 3 beta (GSK3B), vascular endothelial growth factor A (VEGFA), and protein tyrosine kinase 2 (PTK2) genes, which are genes that play a crucial role in phosphatidylinositol 3-kinase (PI3K)-Akt signaling and focal adhesion [57]
Summary
High-risk human papillomavirus (HPV) infection occurs at the basal cell layer of the stratified squamous epithelium (basal keratinocytes) and these viruses are established carcinogens of the cervix, head and neck, anus, penis, vagina and vulva [1]. High-risk HPVs, through the expression of E6, E7 and E5 oncoproteins, are able to immortalize the primary keratinocytes and induce genomic instability [1]. These oncoproteins regulate pathways that induce the hallmarks of cancer, including activation of invasion and metastization [1,2]. One of them is an in silico study by Gutiérrez et al that reports the identification of 19 putative pre-miRNA candidates within HPV genomes [26] Those viral miRNAs, according to their predicted target genes, could promote the development of cervical cancer, by participating in cellular longevity, cell cycle, apoptosis evasion, tissue invasion and metastization [26].
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