锯齿状蛋白1特异性Notch1-磷脂酰肌醇3激酶信号通路对人乳头瘤病毒16型E6和E7的互补作用涉及多效致癌功能，且不依赖于CBF1；Su(H)；Lag-1激活。
Complementation of human papillomavirus type 16 E6 and E7 by Jagged1-specific Notch1-phosphatidylinositol 3-kinase signaling involves pleiotropic oncogenic functions independent of CBF1;Su(H);Lag-1 activation.
作者信息
Veeraraghavalu Karthikeyan, Subbaiah Vanitha K, Srivastava Sweta, Chakrabarti Oishee, Syal Ruchi, Krishna Sudhir
机构信息
National Centre for Biological Sciences, TIFR, UAS-GKVK Campus, Bangalore 560065, India.
出版信息
J Virol. 2005 Jun;79(12):7889-98. doi: 10.1128/JVI.79.12.7889-7898.2005.
Abstract
We have analyzed the induction and role of phosphatidylinositol 3-kinase (PI3K) by Notch signaling in human papillomavirus (HPV)-derived cancers. Jagged1, in contrast to Delta1, is preferentially upregulated in human cervical tumors. Jagged1 and not Delta1 expression sustained in vivo tumors by HPV16 oncogenes in HaCaT cells. Further, Jagged1 expression correlates with the rapid induction of PI3K-mediated epithelial-mesenchymal transition in both HaCaT cells and a human cervical tumor-derived cell line, suggestive of Delta1;Serrate/Jagged;Lag2 ligand-specific roles. Microarray analysis and dominant-negatives reveal that Notch-PI3K oncogenic functions can be independent of CBF1;Su(H);Lag-1 activation and instead relies on Deltex1, an alternative Notch effector.
摘要
我们分析了Notch信号通路在人乳头瘤病毒（HPV）相关癌症中对磷脂酰肌醇3激酶（PI3K）的诱导作用及其角色。与Delta1不同，Jagged1在人宫颈肿瘤中优先上调。在HaCaT细胞中，HPV16致癌基因可在体内肿瘤中维持Jagged1而非Delta1的表达。此外，Jagged1的表达与HaCaT细胞和一种人宫颈肿瘤来源细胞系中PI3K介导的上皮-间质转化的快速诱导相关，提示Delta1、锯齿状蛋白/Jagged1、Lag2配体具有特异性作用。微阵列分析和显性阴性实验表明，Notch-PI3K致癌功能可能独立于CBF1、Su(H)、Lag-1激活，而是依赖于另一种Notch效应分子Deltex1。
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