Abi1 regulates transcriptional activity of androgen receptor by novel dna and ar binding mechanism
AssigneesThe Research Foundation for The State University of New York, The Johns Hopkins University
InventorsLeszek Kotula, Alaji Bah, Dominique Frueh
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Abstract
The embodiments disclosed herein are directed to identifying novel mechanisms of transcription in prostate cancer by a unique DNA binding mechanism involving actin cytoskeleton regulatory protein ABI1. Further embodiments disclosed herein are directed to ABI1-DNA binding activities that predict survival of prostate cancer patients. Moreover, the embodiments disclosed herein are directed to ABI1-AR reciprocal regulation that has far reaching implications for tumor plasticity and androgen-sensitive pathogenesis.
Claims11
A method for selectively treating prostate cancer activity in a human host, said method comprising:
- reducing ABI1 Exon 4 expression in a human host in need of such treatment.
A method for selectively treating prostate cancer activity in a human host, said method comprising:
- administering a compound that selectively inhibits ABI1 Exon 4 expression in a human host in need of such treatment.
A method for selectively inhibiting ABI1 Exon 4 expression activity in a human host, comprising administering a compound that selectively inhibits ABI1 Exon 4 expression in a human host in need of such treatment, wherein the ability of the compound to selectively inhibit the activity of ABI1 Exon 4 expression is determined by:
- a) contacting a genetically engineered cell that expresses human ABI1 Exon 4 expression, with the compound for 30 minutes;
- b) measuring the amount of residues 155-159 produced by the cell;
- and
- c) comparing the amount of residues 155-159 produced by each cell exposed to the compound to the amount of residues 155-159 produced by control cells that were not exposed to the compound, so that the compounds that inhibit production of residues 155-159 are identified.
Dependencies are inferred from the claim text.