癌症研究
下调和上调
癌症
上皮-间质转换
肿瘤进展
NF-κB
转移
癌变
信号转导
激活剂(遗传学)
PI3K/AKT/mTOR通路
化学
生物
医学
细胞生物学
内科学
基因
生物化学
作者
Diego Carrillo-Beltrán,Juan Pablo Muñoz,Nahir Guerrero-Vásquez,Rancés Blanco,Óscar León,Vanesca de Souza Lino,Julio C. Tapia,Edio Maldonado,Karen Dubois-Camacho,Marcela A. Hermoso,Alejandro Corvalán,Gloria M. Calaf,Enrique Boccardo,Francisco Aguayo
出处
期刊:Cancers
[MDPI AG]
日期:2020-07-15
卷期号:12 (7): 1904-1904
被引量:13
标识
DOI:10.3390/cancers12071904
摘要
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-κB), 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-κB. 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-κB 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.
科研通智能强力驱动
Strongly Powered by AbleSci AI