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Am J Translational Res 1(1):62-71,2009
Original Article
Increased expression of histone deacetylaces (HDACs) and inhibition
of prostate cancer growth and invasion by HDAC inhibitor SAHA
Longgui Wang, Xuanyi Zou, Aaron D. Berger, Christian Twiss, Yi Peng, Yirong Li, Jason Chiu, Hongfeng Guo, Jaya
Satagopan, Andrew Wilton, William Gerald, Ross Basch, Iman Osman, Peng Lee
Departments of Urology, Pathology, and Dermatology, New York University School of Medicine, New York Harbor
Healthcare System, Departments of Biostatistics and Pathology, Memorial Sloan Kettering Cancer Center, New
York, NY,
Received October 31, accepted November and available online November, 2008
Abstract: Histone deacetetylases (HDACs) are a group of corepressors of transcriptional activators and their
levels of expression are potentially dysregulated in prostate cancer. Certain inhibitors of histone deacetylases
(HDACs) show anti-tumor activity in prostate cancer cell lines. Here, we systemically studied the expression of
HDACs in human prostate cancer and the suppression of prostate cancer growth and invasion by HDAC inhibitor
SAHA. HDAC1-5 showed increased expression using a combination of DNA microarray, in-situ hybridization, and
immunohistochemistry in benign and malignant human prostate tissue as well as RT-PCR and Western blot
analysis on various PCa cell lines. Importantly, HDAC inhibitor SAHA suppressed, in particular, prostate cancer
cell growth and invasion determined using cell proliferation and Matrigel invasion assays. The findings of this
study show that the expression of HDACs and their associated corepressors are increased in prostate cancer in
humans and HDAC inhibitor SAHA could serve as a potential therapeutic agent in prostate cancer in addition to
antiandrogens. (AJTR810003).
Key Words: Prostate cancer, hormone receptor, androgen, corepressor, microarray, in situ hybridization, histone
deacetylase
Full Text PDF
Address all correspondence to:
Peng Lee MD, PhD
Department of Pathology
New York University School of Medicine
New York Harbor Healthcare System
423 E. 23rd Street, Room 6140N
New York, NY 10010
Tel: 212-951-3418
Fax: 212-951-6341
E-mail: peng.lee@nyumc.org
or Iman Osman, MD
Department of Urology
New York University School of Medicine
E-mail: Iman.osman@nyumc.org
Original Article
Increased expression of histone deacetylaces (HDACs) and inhibition
of prostate cancer growth and invasion by HDAC inhibitor SAHA
Longgui Wang, Xuanyi Zou, Aaron D. Berger, Christian Twiss, Yi Peng, Yirong Li, Jason Chiu, Hongfeng Guo, Jaya
Satagopan, Andrew Wilton, William Gerald, Ross Basch, Iman Osman, Peng Lee
Departments of Urology, Pathology, and Dermatology, New York University School of Medicine, New York Harbor
Healthcare System, Departments of Biostatistics and Pathology, Memorial Sloan Kettering Cancer Center, New
York, NY,
Received October 31, accepted November and available online November, 2008
Abstract: Histone deacetetylases (HDACs) are a group of corepressors of transcriptional activators and their
levels of expression are potentially dysregulated in prostate cancer. Certain inhibitors of histone deacetylases
(HDACs) show anti-tumor activity in prostate cancer cell lines. Here, we systemically studied the expression of
HDACs in human prostate cancer and the suppression of prostate cancer growth and invasion by HDAC inhibitor
SAHA. HDAC1-5 showed increased expression using a combination of DNA microarray, in-situ hybridization, and
immunohistochemistry in benign and malignant human prostate tissue as well as RT-PCR and Western blot
analysis on various PCa cell lines. Importantly, HDAC inhibitor SAHA suppressed, in particular, prostate cancer
cell growth and invasion determined using cell proliferation and Matrigel invasion assays. The findings of this
study show that the expression of HDACs and their associated corepressors are increased in prostate cancer in
humans and HDAC inhibitor SAHA could serve as a potential therapeutic agent in prostate cancer in addition to
antiandrogens. (AJTR810003).
Key Words: Prostate cancer, hormone receptor, androgen, corepressor, microarray, in situ hybridization, histone
deacetylase
Full Text PDF
Address all correspondence to:
Peng Lee MD, PhD
Department of Pathology
New York University School of Medicine
New York Harbor Healthcare System
423 E. 23rd Street, Room 6140N
New York, NY 10010
Tel: 212-951-3418
Fax: 212-951-6341
E-mail: peng.lee@nyumc.org
or Iman Osman, MD
Department of Urology
New York University School of Medicine
E-mail: Iman.osman@nyumc.org
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