In an article published online on January 18, 2012 in Cancer Research, Professor of Cancer Biology, Urology and Radiation Oncology Karen Knudsen, PhD and her associates at Thomas Jefferson University report a benefit for curcumin, an isoflavone found in the spice turmeric, in reducing the growth of castration-resistant prostate cancer in men undergoing androgen deprivation therapy. Androgen deprivation therapy is a treatment for prostate cancer that works by inhibiting the androgen receptor. While androgen deprivation therapy is effective in many cases of prostate cancer, the disease often becomes resistant to therapy due to reactivation of the androgen receptor, necessitating other methods of treatment.
"Nuclear receptors and pioneer factors drive the development and progression of prostate cancer," the authors write. "In this disease, aggressive disease phenotypes and hormone therapy failures result from resurgent activity of androgen receptor and the upregulation of coactivator protein p300 and pioneer factors. Thus, a major current emphasis in the field is to identify mechanisms by which castrate-resistant androgen receptor activity and pioneer factor function can be combinatorially suppressed."
In preliminary research, curcumin was found to suppress the nuclear receptor activators p300 and CREB1-binding protein (CBP), which work against androgen deprivation therapy. For the current study, Dr Knudsen's team utilized prostate cancer cells subjected to androgen deprivation, and found that the addition of physiologically attainable doses of curcumin resulted in cell cycle inhibition and a reduction in survival compared to cancer cells that did not receive curcumin. In another experiment using mice that were castrated and implanted with prostate tumors, animals that received curcumin experienced decreased tumor growth and mass compared with untreated mice.
"This study sets the stage for further development of curcumin as a novel agent to target androgen receptor signaling," Dr Knudsen stated. "It also has implications beyond prostate cancer since p300 and CBP are important in other malignancies, like breast cancer. In tumors where these play an important function, curcumin may prove to be a promising therapeutic agent."
"Nuclear receptors and pioneer factors drive the development and progression of prostate cancer," the authors write. "In this disease, aggressive disease phenotypes and hormone therapy failures result from resurgent activity of androgen receptor and the upregulation of coactivator protein p300 and pioneer factors. Thus, a major current emphasis in the field is to identify mechanisms by which castrate-resistant androgen receptor activity and pioneer factor function can be combinatorially suppressed."
In preliminary research, curcumin was found to suppress the nuclear receptor activators p300 and CREB1-binding protein (CBP), which work against androgen deprivation therapy. For the current study, Dr Knudsen's team utilized prostate cancer cells subjected to androgen deprivation, and found that the addition of physiologically attainable doses of curcumin resulted in cell cycle inhibition and a reduction in survival compared to cancer cells that did not receive curcumin. In another experiment using mice that were castrated and implanted with prostate tumors, animals that received curcumin experienced decreased tumor growth and mass compared with untreated mice.
"This study sets the stage for further development of curcumin as a novel agent to target androgen receptor signaling," Dr Knudsen stated. "It also has implications beyond prostate cancer since p300 and CBP are important in other malignancies, like breast cancer. In tumors where these play an important function, curcumin may prove to be a promising therapeutic agent."
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