期刊
VIROLOGY
卷 478, 期 -, 页码 50-60出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2015.02.002
关键词
HPV E6; Keratinocytes; NFX1-123; Notch; Differentiation; Cell cycle
类别
资金
- NIH [R01 CA 172742A1]
High-risk human papillomavirus (HR HPV) oncoproteins bind host cell proteins to dysregulate and uncouple apoptosis, senescence, differentiation, and growth. These pathways are important for both the viral life cycle and cancer development. HR HPV16 E6 (16E6) interacts with the cellular protein NFX1-123, and they collaboratively increase the growth and differentiation master regulator, Notchl. In 16E6 expressing keratinocytes (16E6 HEKs), the Notch canonical pathway genes Hes1 and Hes5 were increased with overexpression of NFX1-123, and their expression was directly linked to the activation or blockade of the Notchl receptor. Keratinocyte differentiation genes Keratin 1 and Keratin 10 were also increased, but in contrast their upregulation was only indirectly associated with Notchl receptor stimulation and was fully unlinked to growth arrest, increased p21(waf1/CIP1), or decreased proliferative factor Ki67. This leads to a model of 16E6, NFX1-123, and Notchl differently regulating canonical and differentiation pathways and entirely uncoupling cellular arrest from increased differentiation. (C) 2015 Elsevier Inc. All rights reserved.
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