The role of human papillomavirus oncoproteins E6 and E7 in apoptosis

被引：80

作者：

Finzer, P

Aguilar-Lemarroy, A

Rösl, F

机构：

[1] Deutsch Krebsforschungszentrum, Forschungsschwerpunkt Angew Tumorvirol, Abt Tumorvirusimmunol, D-69120 Heidelberg, Germany

[2] Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, France

来源：

CANCER LETTERS | 2002年 / 188卷 / 1-2期

关键词：

CD95/tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)/TNF-alpha pathway; immunological escape; antiviral host defense; cervical cancer; histone deacetylases (HDAC); sodium butyrate; p53; pRb; E2F;

D O I：

10.1016/S0304-3835(02)00431-7

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The oncogenic potential of 'high risk' human papillomaviruses can be mainly attributed to two small proteins called E6 and ET Even these oncoproteins have a low molecular size, they are highly promiscuous and are capable to interact with a whole variety of host cellular regulator proteins to elicit cellular immortalization and ultimately complete malignant transformation. To avoid reiterations in summarizing the biochemical and molecular biological properties of E6/E7 in terms of their influence on cell cycle control, the present review is mainly an attempt to describe some regulatory principles by which human papillomavirus (HPV) oncoproteins can interfere with apoptosis in order to escape immunological surveillance during progression to cervical cancer. The models derived from these basic cellular and molecular studies are relevant to our understanding of HPV-induced carcinogenesis. Conversely, experimental procedures aimed at relieving apoptosis resistance, can facilitate the eradication of immunologically suspicious cells and may prevent the accumulation of cervical intraepithelial cell abnormalities in future prophylactic or therapeutic approaches. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：15 / 24

页数：10

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