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J. Biol. Chem., Vol. 283, Issue 28, 99934, July 11, 2008

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RNA Polymerase III and Cancer

RNA polymerase III transcription, responsible for synthesizing many un-translated RNAs such as 5 S ribosomal and transfer RNA, is deregulated in tumor cells, although it's not known if this is a cause or consequence of cell transformation. In this Paper of the Week, Sandra Johnson and colleagues demonstrate that enhanced RNA pol III transcription is indeed required, although not sufficient, for full tumor potential. In oncogenic fibroblasts displaying enhanced RNA pol III activity (via TBP (TATA-binding protein) or c-Myc activation), decreasing the expression of the pol III transcription factor Brf1 could subsequently decrease pol III transcription. Although Brf1 suppression did not slow down the proliferation of the transformed fibroblasts, it did prevent anchorage-independent tumor growth in soft agar and tumor formation in mice. On the other hand, increasing Brf1 expression in normal cells could not by itself promote cellular transformation, suggesting that enhanced pol III activity works in concert with other factors in tumorigenesis. Johnson and colleagues believe this work should solidify RNA pol III machinery as a viable target in anti-cancer therapy.

Although suppressing the RNA pol III transcription factor Brf1 doesn't slow down cell proliferation in cancer cells (left), it does significantly reduce anchorage-independent colony growth (right).

FOOTNOTES

See referenced article, J. Biol. Chem. 2008, 283, 19184-19191

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This Article Full Text (PDF) Author Profile Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Related Collections Papers Of The Week Social Bookmarking                      What's this?