Human papillomavirus 16E6 and NFX1-123 potentiate Notch signaling and differentiation without activating cellular arrest.
Human papillomavirus 16E6 and NFX1-123 potentiate Notch signaling and differentiation without activating cellular arrest.
复制标题
DOI：
10.1016/j.virol.2015.02.002
复制
发表时间：
2015-04
期刊：
影响因子：
3.7
通讯作者：
Katzenellenbogen, Rachel A.
中科院分区：
文献类型：
--
作者：
Vliet-Gregg, Portia A.;Hamilton, Jennifer R.;Katzenellenbogen, Rachel A.
高危人乳头瘤病毒 (HR HPV) 癌蛋白与宿主细胞蛋白结合，从而失调和解开细胞凋亡、衰老、分化和生长。这些途径对于病毒生命周期和癌症发展都很重要。 HR HPV16 E6 (16E6) 与细胞蛋白 NFX1-123 相互作用，它们协同增加生长和分化主调节因子 Notch1。在表达16E6的角质形成细胞（16E6 HFK）中，Notch经典途径基因Hes1和Hes5随着NFX1-123的过度表达而增加，并且它们的表达与Notch1受体的激活或阻断直接相关。角质形成细胞分化基因 Keratin 1 和 Keratin 10 也增加，但相反，它们的上调仅与 Notch1 受体刺激间接相关，与生长停滞、p21Waf1/CIP1 增加或增殖因子 Ki67 减少完全无关。这导致了 16E6、NFX1-123 和 Notch1 的模型不同地调节规范和分化途径，并完全解除细胞停滞与分化增加的耦合。
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, Notch1. In 16E6 expressing keratinocytes (16E6 HFKs), 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 Notch1 receptor. Keratinocyte differentiation genes Keratin 1 and Keratin 10 were also increased, but in contrast their upregulation was only indirectly associated with Notch1 receptor stimulation and was fully unlinked to growth arrest, increased p21Waf1/CIP1, or decreased proliferative factor Ki67. This leads to a model of 16E6, NFX1-123, and Notch1 differently regulating canonical and differentiation pathways and entirely uncoupling cellular arrest from increased differentiation.
登录
查看更多内容
影响因子：
5.4
作者：
Katzenellenbogen, Rachel A.;Egelkrout, Erin M.;Galloway, Denise A.
通讯作者：
Galloway, Denise A.
影响因子：
5.4
作者：
Katzenellenbogen, Rachel A.;Vliet-Gregg, Portia;Galloway, Denise A.
通讯作者：
Galloway, Denise A.
影响因子：
64.5
作者：
SCHEFFNER, M;HUIBREGTSE, JM;HOWLEY, PM
通讯作者：
HOWLEY, PM
影响因子：
5.5
作者：
Moscicki AB;Schiffman M;Burchell A;Albero G;Giuliano AR;Goodman MT;Kjaer SK;Palefsky J
通讯作者：
Palefsky J
影响因子：
1.3
作者：
Branca, M.;Giorgi, C.;Syrjanen, K.
通讯作者：
Syrjanen, K.