Bmi1 promotes prostate tumorigenesis via inhibiting p16INK4A and p14ARF expression
Copyright policy )Bmi1 promotes prostate tumorigenesis via inhibiting p16INK4A and p14ARF expression
We report here that the polycomb group protein Bmi1 promotes prostate tumorigenesis. Bmi1 is detected at higher levels in androgen-independent PC3 and DU145 than in androgen-dependent LNCaP prostate cancer (CaP) cells. Ectopic Bmi1 enhanced the expression of human telomerase reverse transcriptase (hTERT) and suppressed the exression of p16(INK4A) and p14(ARF) in CaP cells. Consistent with these observations, immunohistochemical staining of 51 cases of primary CaP specimens revealed 1.4 fold (p=0.014) and 1.3 fold (p=0.051) higher levels of Bmi1-positive cells in carcinoma compared to normal prostatic epithelial cells and PIN, respectively. In primary CaPs, Bmi1 expression was associated with a reduction in p16(INK4A) and p14(ARF). Furthermore, in comparison to empty vector-transfected cells, Bmi1-expressing DU145 cells formed significantly larger tumors in NOD/SCID mice. Taken together, we demonstrate that Bmi1 promotes prostate tumorigenesis.
- Covenant Health System United States
- St. Joseph Hospital United States
- McMaster University (McMaster Centre for Software Certification) Canada
- St. Joseph's Hospital Canada
- McMaster University Canada
Male, Polycomb Repressive Complex 1, Prostate cancer, Nuclear Proteins, Prostatic Neoplasms, p14ARF, Bmi1, Immunohistochemistry, Repressor Proteins, Mice, p16INK4A, Cell Line, Tumor, Proto-Oncogene Proteins, Tumor Suppressor Protein p14ARF, Molecular Medicine, Animals, Humans, Molecular Biology, Cyclin-Dependent Kinase Inhibitor p16
Male, Polycomb Repressive Complex 1, Prostate cancer, Nuclear Proteins, Prostatic Neoplasms, p14ARF, Bmi1, Immunohistochemistry, Repressor Proteins, Mice, p16INK4A, Cell Line, Tumor, Proto-Oncogene Proteins, Tumor Suppressor Protein p14ARF, Molecular Medicine, Animals, Humans, Molecular Biology, Cyclin-Dependent Kinase Inhibitor p16
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