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Accession Number ADA567635
Title Role of p53 in cdk Inhibitor VMY-1-103-Induced Apoptosis in Prostate Cancer.
Publication Date Sep 2012
Media Count 26p
Personal Author L. Ringer
Abstract Cyclin-dependent kinase inhibitor VMY-1-103 induces a G2/M cell cycle arrest and apoptosis in prostate cancer cell lines. Cancer cell lines, including prostate cancer, show a differential sensitivity to VMY-1-103 that correlates with p53 status. In addition, VMY-1-103 sensitivity increases in cancer cell lines as compared with normal cell lines, regardless of p53 status. Knockdown experiments in LNCaP cells show a reduced sensitivity to VMY-1-103 by resulting in a decreased cell death and this result can be rescued by the addition of wild-type p53. Transient transfections of wild-type p53 into p53- null PC-3 cells resulted in increased cell death upon VMY treatment. Furthermore, PRIMA-1 pre-treatment restored p53 activity in p53-mutant DU145 cells and sensitized them to VMY-mediated cell death. As compared with other solid tumors, only a small percentage of prostate cancer cases contain p53 mutations. Therapeutically, this is important as a majority of prostate cancer patients could benefit from VMY.
Keywords Apoptosis
Cells(Biology)
Death
Inhibitors
Phosphorus transferases
Prostate cancer

 
Source Agency Non Paid ADAS
NTIS Subject Category 57A - Anatomy
57S - Physiology
57E - Clinical Medicine
Corporate Author Georgetown Univ., Washington, DC.
Document Type Technical report
Title Note Annual summary 22 Aug 2011-21 Aug 2012.
NTIS Issue Number 1309
Contract Number W81XWH-11-1-0669

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