braco-19 and Prostatic-Neoplasms

braco-19 has been researched along with Prostatic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for braco-19 and Prostatic-Neoplasms

Article	Year
A G-quadruplex telomere targeting agent produces p16-associated senescence and chromosomal fusions in human prostate cancer cells. Molecular cancer therapeutics, 2004, Volume: 3, Issue:10 The trisubstituted acridine derivative BRACO-19 has been designed to interact with and stabilize the quadruplex DNA structures that can be formed by folding of the single-stranded repeats at the 3' end of human telomeres. We suggest that the BRACO-19 complex inhibits the catalytic function of telomerase in human cancer cells and also destabilizes the telomerase-telomere capping complex so that cells enter senescence. Here, we present evidence showing that the inhibition of cell growth caused by BRACO-19 in DU145 prostate cancer cells occurs more rapidly than would be expected solely by the inhibition of the catalytic function of telomerase, and that senescence is accompanied by an initial up-regulation of the cyclin-dependent kinase inhibitor p21, with subsequent increases in p16(INK4a) expression. We also show that treatment with BRACO-19 causes extensive end-to-end chromosomal fusions, consistent with telomere uncapping. Topics: 3T3 Cells; Acridines; Animals; Blotting, Western; Catalysis; Cell Line, Tumor; Cell Proliferation; Cellular Senescence; Chromosomes; Cyclin-Dependent Kinase Inhibitor p16; DNA; G-Quadruplexes; Humans; Ligands; Male; Metaphase; Mice; Models, Chemical; Nucleic Acid Conformation; Prostatic Neoplasms; Rhodamines; Telomerase; Telomere; Time Factors; Up-Regulation	2004

Article

Year

A G-quadruplex telomere targeting agent produces p16-associated senescence and chromosomal fusions in human prostate cancer cells.

Molecular cancer therapeutics, 2004, Volume: 3, Issue:10

The trisubstituted acridine derivative BRACO-19 has been designed to interact with and stabilize the quadruplex DNA structures that can be formed by folding of the single-stranded repeats at the 3' end of human telomeres. We suggest that the BRACO-19 complex inhibits the catalytic function of telomerase in human cancer cells and also destabilizes the telomerase-telomere capping complex so that cells enter senescence. Here, we present evidence showing that the inhibition of cell growth caused by BRACO-19 in DU145 prostate cancer cells occurs more rapidly than would be expected solely by the inhibition of the catalytic function of telomerase, and that senescence is accompanied by an initial up-regulation of the cyclin-dependent kinase inhibitor p21, with subsequent increases in p16(INK4a) expression. We also show that treatment with BRACO-19 causes extensive end-to-end chromosomal fusions, consistent with telomere uncapping.

Topics: 3T3 Cells; Acridines; Animals; Blotting, Western; Catalysis; Cell Line, Tumor; Cell Proliferation; Cellular Senescence; Chromosomes; Cyclin-Dependent Kinase Inhibitor p16; DNA; G-Quadruplexes; Humans; Ligands; Male; Metaphase; Mice; Models, Chemical; Nucleic Acid Conformation; Prostatic Neoplasms; Rhodamines; Telomerase; Telomere; Time Factors; Up-Regulation

2004