Orthogonal ubiquitin transfer reveals human papillomavirus E6 downregulates nuclear transport to disarm interferon‐γ dependent apoptosis of cervical cancer cells

2021 ◽  
Vol 35 (11) ◽  
Author(s):  
Yiyang Wang ◽  
Ruochuan Liu ◽  
Jia Liao ◽  
Lucen Jiang ◽  
Geon H. Jeong ◽  
...  
Tumor Biology ◽  
2016 ◽  
Vol 37 (10) ◽  
pp. 13137-13154 ◽  
Author(s):  
Kanchan Vishnoi ◽  
Sutapa Mahata ◽  
Abhishek Tyagi ◽  
Arvind Pandey ◽  
Gaurav Verma ◽  
...  

2007 ◽  
Vol 175 (2) ◽  
pp. 132-137 ◽  
Author(s):  
Christine F.W. Vermeulen ◽  
Ekaterina S. Jordanova ◽  
Károly Szuhai ◽  
Sandra Kolkman-Uljee ◽  
M. Albert Vrede ◽  
...  

2005 ◽  
Vol 68 (5) ◽  
pp. 1311-1319 ◽  
Author(s):  
Lisa N. Putral ◽  
Megan J. Bywater ◽  
Wenyi Gu ◽  
Nicholas A. Saunders ◽  
Brian G. Gabrielli ◽  
...  

2001 ◽  
Vol 98 (3) ◽  
pp. 1218-1223 ◽  
Author(s):  
A. Hengstermann ◽  
L. K. Linares ◽  
A. Ciechanover ◽  
N. J. Whitaker ◽  
M. Scheffner

2003 ◽  
Vol 77 (2) ◽  
pp. 1551-1563 ◽  
Author(s):  
Rosa Anna DeFilippis ◽  
Edward C. Goodwin ◽  
Lingling Wu ◽  
Daniel DiMaio

ABSTRACT Cervical cancer cells express high-risk human papillomavirus (HPV) E6 and E7 proteins, and repression of HPV gene expression causes the cells to cease proliferation and undergo senescence. However, it is not known whether both HPV proteins are required to maintain the proliferative state of cervical cancer cells, or whether mutations that accumulate during carcinogenesis eliminate the need for one or the other of them. To address these questions, we used the bovine papillomavirus E2 protein to repress the expression of either the E6 protein or the E7 protein encoded by integrated HPV18 DNA in HeLa cervical carcinoma cells. Repression of the E7 protein activated the Rb pathway but not the p53 pathway and triggered senescence, whereas repression of the E6 protein activated the p53 pathway but not the Rb pathway and triggered both senescence and apoptosis. Telomerase activity, cyclin-dependent kinase activity, and expression of c-myc were markedly inhibited by repression of either E6 or E7. These results demonstrate that continuous expression of both the E6 and the E7 protein is required for optimal proliferation of cervical carcinoma cells and that the two viral proteins exert distinct effects on cell survival and proliferation. Therefore, strategies that inhibit the expression or activity of either viral protein are likely to inhibit the growth of HPV-associated cancers.


Sign in / Sign up

Export Citation Format

Share Document