Human papillomavirus type 16 E6 and E 7 proteins alter NF-kB in cultured cervical epithelial cells and inhibition of NF-kB promotes cell growth and immortalization.
Human papillomavirus type 16 E6 and E 7 proteins alter NF-kB in cultured cervical epithelial cells and inhibition of NF-kB promotes cell growth and immortalization.
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DOI：
10.1016/j.virol.2011.12.023
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发表时间：
2012-03-30
期刊：
影响因子：
3.7
通讯作者：
Woodworth CD
中科院分区：
文献类型：
--
作者：
Vandermark ER;Deluca KA;Gardner CR;Marker DF;Schreiner CN;Strickland DA;Wilton KM;Mondal S;Woodworth CD
转录因子的NF-kB家族调节重要的生物学功能，包括细胞生长、存活和免疫应答。我们发现，人乳头瘤病毒16型（HPV-16）E7和E6/E7蛋白抑制基础和TNF-α诱导的NF-kB的活性在人类上皮细胞培养的宫颈转化区，解剖区域，大多数宫颈癌的发展。相反，HPV-16 E6以细胞类型和细胞生长依赖性方式调节NF-κ B。NF-kB影响HPV 16诱导的宫颈细胞永生化。通过IkB α阻遏突变体抑制NF-κ B增加了HPV-16的集落形成和永生化。相反，通过组成型表达p65激活NF-κ B抑制增殖和永生化。我们的研究结果表明，HPV-16 E6/E7对NF-kB的抑制有助于宫颈转化区细胞的永生化。
The NF-kB family of transcription factors regulates important biological functions including cell growth, survival and the immune response. We found that Human Papillomavirus type 16 (HPV-16) E7 and E6/E7 proteins inhibited basal and TNF-alpha-inducible NF-kB activity in human epithelial cells cultured from the cervical transformation zone, the anatomic region where most cervical cancers develop. In contrast, HPV-16 E6 regulated NF-kB in a cell type- and cell growth-dependent manner. NF-kB influenced immortalization of cervical cells by HPV16. Inhibition of NF-kB by an IkB alpha repressor mutant increased colony formation and immortalization by HPV-16. In contrast, activation of NF-kB by constitutive expression of p65 inhibited proliferation and immortalization. Our results suggest that inhibition of NF-kB by HPV-16 E6/E7 contributes to immortalization of cells from the cervical transformation zone.
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