| Literature DB >> 27818285 |
Elektra Peta1, Rocco Cappellesso2, Giulia Masi1, Alessandro Sinigaglia3, Marta Trevisan1, Angela Grassi4, Barbara Di Camillo4, Elisa Vassarotto2, Ambrogio Fassina2, Giorgio Palù1, Luisa Barzon5.
Abstract
Dysregulation of host microRNA expression has been involved in the development and progression of human papillomavirus (HPV)-related tumors. Analysis of miR-146a expression in a series of 59 penile squamous cell carcinomas (PSCCs) showed that its levels were lower in high-risk HPV-positive than in HPV-negative PSCCs and inversely correlated with expression of epidermal growth factor receptor (EGFR), a known target for miR-146a. Analysis of genotype distribution for rs2910164, a common functional polymorphism of miR-146a, did not identify correlations with miR-146a levels and EGFR expression in PSCCs. In vitro experiments demonstrated that E6 of HPV type 16, but not low-risk HPV-6, down-regulated miR-146a in human foreskin keratinocytes and up-regulated EGFR. Ectopic expression of miR-146a decreased expression of EGFR and inhibited proliferation of keratinocytes and cervical carcinoma cells. EGFR is commonly overexpressed in penile cancer and in other squamous cell carcinomas. Molecular mechanisms leading to EGFR overexpression and activation are known for HPV-negative cancers and include amplification or mutations of the EGFR gene. The results of this study indicate that down-regulation of miR-146a may represent another mechanism of EGFR overexpression in PSCCs, which can be mediated by high-risk HPV E6 in HPV-related tumors.Entities:
Keywords: E6; Epidermal growth factor receptor; HPV-16; Human papillomavirus; MiR-146a; Penile squamous cell carcinoma
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Year: 2016 PMID: 27818285 DOI: 10.1016/j.humpath.2016.10.019
Source DB: PubMed Journal: Hum Pathol ISSN: 0046-8177 Impact factor: 3.466