The epithelial-mesenchymal transition induced by keratinocyte growth conditions is overcome by E6 and E7 from HPV16, but not HPV8 and HPV38: Characterization of global transcription profiles
The epithelial-mesenchymal transition induced by keratinocyte growth conditions is overcome by E6 and E7 from HPV16, but not HPV8 and HPV38: Characterization of global transcription profiles
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DOI：
10.1016/j.virol.2009.03.033
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发表时间：
2009-06-05
期刊：
影响因子：
3.7
通讯作者：
Gariglio, Marisa
中科院分区：
文献类型：
--
作者：
Azzimonti, Barbara;Dell'Oste, Valentina;Gariglio, Marisa
本研究的目的是评估表达E6和E7蛋白的原代人角质形成细胞在不同培养条件下的生长特性，所述蛋白来自β或α基因型。我们证明，当在含有FAD培养基（F12/DMEM/5%FBS）的塑料上生长时，表达来自HPV 8和38的E6和E7的角质形成细胞不可逆地经历上皮-间充质转化（EMT）。HPV 16 E6/E7的表达能够完全克服FAD诱导的EMT。永生化仅在HPV 16转导的细胞系中观察到，而KerHPV 8和38的更多增殖表型主要与FAD诱导的EMT有关。对指数生长细胞的微阵列分析鉴定了146个细胞基因，这些基因与HPV 8和38转导细胞相比在HPV 16中差异调节。在HPV 16转导的细胞中观察到与表皮发育和分化相关的大量转录物的积累，而在HPV 8和38转导的细胞中，参与细胞外基质、多细胞生物过程和炎症反应的基因的转录物受到影响。(c)2009爱思唯尔公司All rights reserved.
The aim of this Study was to evaluate the growth properties Of primary human keratinocytes expressing E6 and E7 proteins, which are from either the beta- or alpha-genotypes, under different culture conditions. We demonstrated that keratinocytes expressing E6 and E7, from both HPV8 and 38, irreversibly underwent the epithelial-mesenchymal transition (EMT) when grown on plastic with FAD medium (F12/DMEM/5%FBS). Expression of E6/E7 from HPV16 was capable of fully overcoming the FAD-induced EMT. Immortalization was only observed in HPV16-transduced cell lines, while the more proliferating phenotype of both KerHPV8 and 38 was mainly related to FAD-induced EMT. Microarray analysis of exponentially growing cells identified 146 cellular genes that were differentially regulated in HPV16 compared to HPV8- and 38-transduced cells. A large accumulation of transcripts associated with epidermal development and differentiation was observed in HPV16-transduced cells, whereas transcripts of genes involved in the extracellular matrix, multicellular organismal processes, and inflammatory response were affected in HPV8 and 38-transduced cells. (c) 2009 Elsevier Inc. All rights reserved.