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Study proposes new ovarian cancer targets
Date:3/13/2014

ast year in Biology of Reproduction that estrogen upregulates the protein in mouse ovaries and in estrogen-supplemented mouse ovarian tumors. In humans, long-term estrogen hormone replacement therapy has been associated with a greater risk of ovarian cancer.

Cell growth and death

Meanwhile, TAF2 may have its own cancer-related modus operandi. Work by other researchers has shown that TAF2 boosts the expression of a protein called C-SRC, that promotes cell growth and proliferation. Perhaps not surprisingly, other studies have found that C-SRC is overexpressed in ovarian tumors.

"Given these results, it is possible that TAF2 overexpression could increase transcription of C-SRC in some ovarian tumors," the researchers wrote.

But what of TAF9, which unlike its brethren seems to become notably less expressed in ovarian cancers? There, too, there is a suspicious mechanistic connection to ovarian cancer. TAF9 is a co-activator of the protein p53, which promotes cell death, a handy thing to promote in tumors. But p53 activity is also suppressed in ovarian cancer. Together, these changes may help ensure the survival of ovarian cancer cells.

Ribeiro and Freiman readily acknowledge that the case they build is circumstantial, but they argue it is more than enough for cancer researchers to look at TAFs as potential targets in their search for new treatments.

"We've compiled this hypothesis and provided the data that we think is relevant, but there still is much that is not known about it," Ribeiro said.

In the lab now, Ribeiro and Freiman are testing the effects in human ovarian cancer cells of manipulating TAF expression and function.


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Contact: David Orenstein
david_orenstein@brown.edu
401-863-1862
Brown University
Source:Eurekalert  

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