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Papillomavirus' E6 and E7 proteins differentially protect from cell apoptosis.

Women's Health Weekly

| March 06, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 MAR 6 - (NewsRx.com & NewsRx.net) -- According to recent research from the United States, "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 which 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," wrote R.A. Defilippis and colleagues, Yale University, School of Medicine.

The researchers concluded: "These results demonstrate that continuous expression of both the E6 and the E7 protein is required for optimal ...

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Source: HighBeam Research, Papillomavirus' E6 and E7 proteins differentially protect from cell...

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