期刊
CANCERS
卷 12, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/cancers12071904
关键词
papillomavirus; pirin; NF-kappa B; oncoprotein; oral; cancer
类别
资金
- Fondecyt [1161219, 1200656, 1160889, 3190744, 3190723]
- CONICYT-FONDAP [15130011]
- Conicyt [21180901]
- FAPESP [2010/20002-0, 2017/02997-3]
A subset of oral carcinomas is etiologically related to high-risk human papillomavirus (HR-HPV) infection, with HPV16 being the most frequent HR-HPV type found in these carcinomas. The oncogenic role of HR-HPV is strongly dependent on the overexpression of E6 and E7 oncoproteins, which, in turn, induce p53 and pRb degradation, respectively. Additionally, it has been suggested that HR-HPV oncoproteins are involved in the regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B), inducing cancer progression and metastasis. Previously, we reported that HPV16 E7 oncoprotein promotes Pirin upregulation resulting in increased epithelial-mesenchymal transition (EMT) and cell migration, with Pirin being an oxidative stress sensor and activator of NF-kappa B. In this study, we demonstrate the mechanism by which HPV16 E7-mediated Pirin overexpression occurs by promoting EGFR/PI3K/AKT1/NRF2 signaling, thus causing PIR/NF-kappa B activation in oral tumor cells. Our results demonstrate a new mechanism by which E7 contributes to oral cancer progression, proposing PIR as a potential new therapeutic target.
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