Differential androgen receptor signals in different cells explain why androgen-deprivation therapy of prostate cancer fails
Prostate cancer is one of the major causes of cancer-related death in the western world. Androgen-deprivation therapy (ADT) for the suppression of androgens binding to the androgen receptor (AR) has been the norm of prostate cancer treatment. Despite early success to suppress prostate tumor growth,...
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| Veröffentlicht in: | Oncogene 2010-06, Vol.29 (25), p.3593-3604 |
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| creator | Niu, Y Chang, T-M Yeh, S Ma, W-L Wang, Y Z Chang, C |
| description | Prostate cancer is one of the major causes of cancer-related death in the western world. Androgen-deprivation therapy (ADT) for the suppression of androgens binding to the androgen receptor (AR) has been the norm of prostate cancer treatment. Despite early success to suppress prostate tumor growth, ADT eventually fails leading to recurrent tumor growth in a hormone-refractory manner, even though AR remains to function in hormone-refractory prostate cancer. Interestingly, some prostate cancer survivors who received androgen replacement therapy had improved quality of life without adverse effect on their cancer progression. These contrasting clinical data suggest that differential androgen/AR signals in individual cells of prostate tumors can exist in the same or different patients, and may be used to explain why ADT of prostate cancer fails. Such a hypothesis is supported by the results obtained from transgenic mice with selective knockout of AR in prostatic stromal vs epithelial cells and orthotopic transplants of various human prostate cancer cell lines with AR over-expression or knockout. These studies concluded that AR functions as a stimulator for prostate cancer proliferation and metastasis in stromal cells, as a survival factor of prostatic cancer epithelial luminal cells, and as a suppressor for prostate cancer basal intermediate cell growth and metastasis. These dual yet opposite functions of the stromal and epithelial AR may challenge the current ADT to battle prostate cancer and should be taken into consideration when developing new AR-targeting therapies in selective prostate cancer cells. |
| doi_str_mv | 10.1038/onc.2010.121 |
| format | Article |
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Androgen-deprivation therapy (ADT) for the suppression of androgens binding to the androgen receptor (AR) has been the norm of prostate cancer treatment. Despite early success to suppress prostate tumor growth, ADT eventually fails leading to recurrent tumor growth in a hormone-refractory manner, even though AR remains to function in hormone-refractory prostate cancer. Interestingly, some prostate cancer survivors who received androgen replacement therapy had improved quality of life without adverse effect on their cancer progression. These contrasting clinical data suggest that differential androgen/AR signals in individual cells of prostate tumors can exist in the same or different patients, and may be used to explain why ADT of prostate cancer fails. Such a hypothesis is supported by the results obtained from transgenic mice with selective knockout of AR in prostatic stromal vs epithelial cells and orthotopic transplants of various human prostate cancer cell lines with AR over-expression or knockout. These studies concluded that AR functions as a stimulator for prostate cancer proliferation and metastasis in stromal cells, as a survival factor of prostatic cancer epithelial luminal cells, and as a suppressor for prostate cancer basal intermediate cell growth and metastasis. These dual yet opposite functions of the stromal and epithelial AR may challenge the current ADT to battle prostate cancer and should be taken into consideration when developing new AR-targeting therapies in selective prostate cancer cells.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2010.121</identifier><identifier>PMID: 20440270</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/322 ; 631/80/86/2363 ; 692/699/67/589/466 ; 692/700/565/1331/238 ; Androgen receptors ; Androgens ; Androgens - metabolism ; Androgens - therapeutic use ; Animals ; Apoptosis ; Biological and medical sciences ; Care and treatment ; Cell Biology ; Cell physiology ; Cell proliferation ; Cell receptors ; Cell structures and functions ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cells ; Cellular signal transduction ; Development and progression ; Disease Progression ; Epithelial cells ; Fundamental and applied biological sciences. Psychology ; Genetic aspects ; Health aspects ; Hormone replacement therapy ; Hormone therapy ; Human Genetics ; Humans ; Internal Medicine ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Metastases ; Metastasis ; Miscellaneous ; Molecular and cellular biology ; Nephrology. Urinary tract diseases ; Neurons ; Oncology ; Overexpression ; Prostate cancer ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Prostatic Neoplasms - therapy ; Quality of life ; Receptors, Androgen - metabolism ; review ; Signal Transduction ; Stromal cells ; Survival factor ; Transgenic mice ; Treatment Outcome ; Tumor cell lines ; Tumors of the urinary system ; Urinary tract. 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Androgen-deprivation therapy (ADT) for the suppression of androgens binding to the androgen receptor (AR) has been the norm of prostate cancer treatment. Despite early success to suppress prostate tumor growth, ADT eventually fails leading to recurrent tumor growth in a hormone-refractory manner, even though AR remains to function in hormone-refractory prostate cancer. Interestingly, some prostate cancer survivors who received androgen replacement therapy had improved quality of life without adverse effect on their cancer progression. These contrasting clinical data suggest that differential androgen/AR signals in individual cells of prostate tumors can exist in the same or different patients, and may be used to explain why ADT of prostate cancer fails. Such a hypothesis is supported by the results obtained from transgenic mice with selective knockout of AR in prostatic stromal vs epithelial cells and orthotopic transplants of various human prostate cancer cell lines with AR over-expression or knockout. These studies concluded that AR functions as a stimulator for prostate cancer proliferation and metastasis in stromal cells, as a survival factor of prostatic cancer epithelial luminal cells, and as a suppressor for prostate cancer basal intermediate cell growth and metastasis. These dual yet opposite functions of the stromal and epithelial AR may challenge the current ADT to battle prostate cancer and should be taken into consideration when developing new AR-targeting therapies in selective prostate cancer cells.</description><subject>631/67/322</subject><subject>631/80/86/2363</subject><subject>692/699/67/589/466</subject><subject>692/700/565/1331/238</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Androgens - metabolism</subject><subject>Androgens - therapeutic use</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>Cell physiology</subject><subject>Cell proliferation</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cells</subject><subject>Cellular signal transduction</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>Epithelial cells</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Hormone replacement therapy</subject><subject>Hormone therapy</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Miscellaneous</subject><subject>Molecular and cellular biology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Neurons</subject><subject>Oncology</subject><subject>Overexpression</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Prostatic Neoplasms - therapy</subject><subject>Quality of life</subject><subject>Receptors, Androgen - metabolism</subject><subject>review</subject><subject>Signal Transduction</subject><subject>Stromal cells</subject><subject>Survival factor</subject><subject>Transgenic mice</subject><subject>Treatment Outcome</subject><subject>Tumor cell lines</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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Androgen-deprivation therapy (ADT) for the suppression of androgens binding to the androgen receptor (AR) has been the norm of prostate cancer treatment. Despite early success to suppress prostate tumor growth, ADT eventually fails leading to recurrent tumor growth in a hormone-refractory manner, even though AR remains to function in hormone-refractory prostate cancer. Interestingly, some prostate cancer survivors who received androgen replacement therapy had improved quality of life without adverse effect on their cancer progression. These contrasting clinical data suggest that differential androgen/AR signals in individual cells of prostate tumors can exist in the same or different patients, and may be used to explain why ADT of prostate cancer fails. Such a hypothesis is supported by the results obtained from transgenic mice with selective knockout of AR in prostatic stromal vs epithelial cells and orthotopic transplants of various human prostate cancer cell lines with AR over-expression or knockout. These studies concluded that AR functions as a stimulator for prostate cancer proliferation and metastasis in stromal cells, as a survival factor of prostatic cancer epithelial luminal cells, and as a suppressor for prostate cancer basal intermediate cell growth and metastasis. These dual yet opposite functions of the stromal and epithelial AR may challenge the current ADT to battle prostate cancer and should be taken into consideration when developing new AR-targeting therapies in selective prostate cancer cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20440270</pmid><doi>10.1038/onc.2010.121</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0950-9232 1476-5594 |
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| subjects | 631/67/322 631/80/86/2363 692/699/67/589/466 692/700/565/1331/238 Androgen receptors Androgens Androgens - metabolism Androgens - therapeutic use Animals Apoptosis Biological and medical sciences Care and treatment Cell Biology Cell physiology Cell proliferation Cell receptors Cell structures and functions Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cells Cellular signal transduction Development and progression Disease Progression Epithelial cells Fundamental and applied biological sciences. Psychology Genetic aspects Health aspects Hormone replacement therapy Hormone therapy Human Genetics Humans Internal Medicine Male Medical sciences Medicine Medicine & Public Health Metastases Metastasis Miscellaneous Molecular and cellular biology Nephrology. Urinary tract diseases Neurons Oncology Overexpression Prostate cancer Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Prostatic Neoplasms - therapy Quality of life Receptors, Androgen - metabolism review Signal Transduction Stromal cells Survival factor Transgenic mice Treatment Outcome Tumor cell lines Tumors of the urinary system Urinary tract. Prostate gland |
| title | Differential androgen receptor signals in different cells explain why androgen-deprivation therapy of prostate cancer fails |
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