TY - JOUR
T1 - Androgen receptor expression in prostate cancer stem cells
T2 - Is there a conundrum?
AU - Sharifi, Nima
AU - Hurt, Elaine M.
AU - Farrar, William L.
N1 - Funding Information:
This research was supported in part by the Intramural Research Program of the NIH, National Cancer Institute. The content of this publication does not necessarily reXect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.
PY - 2008/10
Y1 - 2008/10
N2 - Androgen deprivation therapy (ADT) is standard frontline therapy for metastatic prostate cancer. However, prostate cancer progresses to a castrate-resistant state. The response of prostate cancer to androgen deprivation is mediated by the androgen receptor (AR). Castrate-resistant disease is marked by a gain-of-function in AR and AR reactivation. The stem cell hypothesis of cancer would therefore predict that AR should be expressed in the prostate cancer stem cell, since genetic selection for gain-of-function changes in AR, such as AR gene amplification, should occur at the level of the stem cell population. Initial reports characterizing prostate cancer stem cells suggest that AR is not expressed in this population, which is an apparent conundrum. Here, we examined the CD44+/24- LNCaP putative stem cell population by in-cell Western and show that AR is expressed at the protein level. Our findings suggest that at least a subset of prostate cancers express AR in the putative stem cell population.
AB - Androgen deprivation therapy (ADT) is standard frontline therapy for metastatic prostate cancer. However, prostate cancer progresses to a castrate-resistant state. The response of prostate cancer to androgen deprivation is mediated by the androgen receptor (AR). Castrate-resistant disease is marked by a gain-of-function in AR and AR reactivation. The stem cell hypothesis of cancer would therefore predict that AR should be expressed in the prostate cancer stem cell, since genetic selection for gain-of-function changes in AR, such as AR gene amplification, should occur at the level of the stem cell population. Initial reports characterizing prostate cancer stem cells suggest that AR is not expressed in this population, which is an apparent conundrum. Here, we examined the CD44+/24- LNCaP putative stem cell population by in-cell Western and show that AR is expressed at the protein level. Our findings suggest that at least a subset of prostate cancers express AR in the putative stem cell population.
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U2 - 10.1007/s00280-007-0659-5
DO - 10.1007/s00280-007-0659-5
M3 - Article
C2 - 18075739
AN - SCOPUS:49749086189
SN - 0344-5704
VL - 62
SP - 921
EP - 923
JO - Cancer Chemotherapy and Pharmacology
JF - Cancer Chemotherapy and Pharmacology
IS - 5
ER -