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Cellular, Molecular, and Tumor Biology 111: Regulation of Apoptosis II

The anti-apoptotic protein Mcl-1 is overexpressed in prostate cancer

Karina Pfeil, Iris E. Eder, Jasmin Bektic, Heidi Huebl, Armin Pycha, Georg Schaefer, Hermann Rogatsch, Georg Bartsch and Helmut Klocker
Karina Pfeil
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Iris E. Eder
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Jasmin Bektic
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Heidi Huebl
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Armin Pycha
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Georg Schaefer
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Hermann Rogatsch
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Georg Bartsch
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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Helmut Klocker
Medical University of Innsbruck, Innsbruck, Austria and Lorenz Boehler Krankenhaus Bolzano, Bolzano, Italy
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DOI:  Published April 2004
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Proc Amer Assoc Cancer Res, Volume 45, 2004

Abstract

5172

Therapy escape and progression of prostate cancer is associated with enhanced survival signals and resistance to induction of apoptosis (programmed cell death). Mcl-1 (myeloid cell lymphoma 1) is an anti-apoptotic protein of the Bcl-2 family, which functions in the regulation of apoptosis. We investigated its role in prostate cancer, employing measurement of expression in tumor specimens and regulation of expression in the LNCaP prostate cancer progression model. The androgen-sensitive prostate cancer prostate LNCaP and its long-term androgen ablated sublines LNCaP-abl and LNCaP-abl HOF - the latter two representing advanced prostate cancer - were used to analyze regulation of expression of Mcl-1 and the inpact on induction of apoptosis. Expression levels in the different stages of prostate cancer were determined by immunohistochemistry. Tissue specimens were obtained from prostate cancer patients undergoing radical prostatectomy, from palliative transurethral resections performed after development of hormone-resistant tumors and from distant metastasis removed surgically for palliative reasons. Simulation of long-term androgen ablation therapy in cell culture using LNCaP cells results in upregulation of MCl-1 expression. Regulation of expression involves the protein kinase B (PKB) survival pathway. Mcl-1 levels decrease after inhibition of PKB in LNCaP cell. Most interestingly this downregulation is not seen in the long-term androgen ablated LNCaP-abl cells. Mcl-1 is rarely expressed in benign epithelium, however, in the fast majority of prostate tumors. Immunohistochemistry revealed expression in only 1 of 14 benign specimens, but 59 of 67(88%) primary tumors, in all of 24 local recurrent tumors, in all of 11 lymph node metastases and in 7 of 8 bone metastases specimens. Comparison of non-malignant primary epithelial prostate cells with metastatic cancer cell lines confirmed an increase of Mcl-1 expression in the tumor cells.In conclusion, Mcl-1 overexpression is an early event in prostate cancer suggesting it as a potential target for tumor therapy. This is accompanied by dysregulation of expression during progression. It will be important to understand the interplay of Mcl-1 with the other proteins that regulate the induction of apoptosis.

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April 2004
Volume 64, Issue 7 Supplement
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The anti-apoptotic protein Mcl-1 is overexpressed in prostate cancer
Karina Pfeil, Iris E. Eder, Jasmin Bektic, Heidi Huebl, Armin Pycha, Georg Schaefer, Hermann Rogatsch, Georg Bartsch and Helmut Klocker
Cancer Res April 1 2004 (64) (7 Supplement) 1193;

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The anti-apoptotic protein Mcl-1 is overexpressed in prostate cancer
Karina Pfeil, Iris E. Eder, Jasmin Bektic, Heidi Huebl, Armin Pycha, Georg Schaefer, Hermann Rogatsch, Georg Bartsch and Helmut Klocker
Cancer Res April 1 2004 (64) (7 Supplement) 1193;
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