Oncogenic potential diverge among human papillomavirus type 16 natural variants

被引:45
作者
Sichero, Laura [1 ,2 ]
Simao Sobrinho, Joao [1 ,2 ]
Villa, Luisa Lina [1 ,2 ,3 ]
机构
[1] Ludwig Inst Canc Res, Dept Virol, BR-01323903 Sao Paulo, Brazil
[2] ICESP, Mol Biol Lab, Ctr Translat Oncol, BR-01246000 Sao Paulo, Brazil
[3] Univ Sao Paulo, Dept Radiol, Sch Med, BR-05508 Sao Paulo, Brazil
关键词
Human papillomavirus; HPV-16; Molecular variants; Immortalization; Oncogenic potential; Gene expression; CERVICAL INTRAEPITHELIAL NEOPLASIA; HUMAN KERATINOCYTES; GENE-EXPRESSION; E6; VARIANTS; CANCER; RISK; P53; PROGRESSION; HUMAN-PAPILLOMAVIRUS-16; DIFFERENTIATION;
D O I
10.1016/j.virol.2012.06.011
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
We compared E6/E7 protein properties of three different HPV-16 variants: AA. E-P and E-350G. Primary human foreskin keratinocytes (PHFK) were transduced with HPV-16 E6 and E7 and evaluated for proliferation and ability to grow in soft agar. E-P infected keratinocytes presented the lowest efficiency in colony formation. AA and E-350G keratinocytes attained higher capacity for in vitro transformation. We observed similar degradation of TP53 among HPV-16 variants. Furthermore, we accessed the expression profile in early (p5) and late passage (p30) transduced cells of 84 genes commonly involved in carcinogenesis. Most differences could be attributed to HPV-16 E6/E7 expression. In particular, we detected different expression of ITGA2 and CHEK2 in keratinocytes infected with AA and AA/E-350G late passage cells, respectively, and higher expression of MAP2K1 in E-350G transduced keratinocytes. Our results indicate differences among HPV-16 variants that could explain, at least in part, differences in oncogenic potential attributed to these variants. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:127 / 132
页数:6
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