The Experts below are selected from a list of 129 Experts worldwide ranked by ideXlab platform
Marcella Motta - One of the best experts on this subject based on the ideXlab platform.
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the androgen Derivative 5α androstane 3β 17β diol inhibits prostate cancer cell migration through activation of the estrogen receptor β subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Eugenia Scaccianoce, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5α-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor–independent mechanism. We have shown that the dihydroTestosterone metabolite 5α-androstane-3β,17β-diol (3β-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor β (ERβ), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERβ signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERβ activation in prostate cancer cells. Moreover, 3β-Adiol, through ERβ, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3β-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that ( a ) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and ( b ) that the estrogenic effect of Testosterone Derivatives (ERβ-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3β-hydroxysteroid dehydrogenases (the enzymes responsible for 3β-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol inhibits prostate cancer cell migration through activation of the estrogen receptor beta subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Benita S Katzenellenbogen, Eugenia Scaccianoce, Paolo Martini, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5alpha-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor-independent mechanism. We have shown that the dihydroTestosterone metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor beta (ERbeta), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERbeta signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERbeta activation in prostate cancer cells. Moreover, 3beta-Adiol, through ERbeta, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3beta-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that (a) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and (b) that the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3beta-hydroxysteroid dehydrogenases (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol 3beta adiol inhibits migration of prostate cancer cell by activation of the estrogen receptor beta
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Marcella Motta, Angelo PolettiAbstract:297 In earlier stages, prostate cancer (PC) depends on androgens and may be reduced with androgen blockade. Androgen-ablation therapy often induces androgen-independent PC, characterized by an increased invasiveness. We have found that the the Testosterone Derivative, dihydroTestosterone inhibits cell migration with an androgen receptor (AR)-independent mechanism. This effect has been linked to its metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind AR, but interact with the estrogen receptor beta (ERbeta). 3beta-Adiol inhibits cell migration of PC through the activation of the ERbeta signalling, while estradiol is not active, suggesting the existence of different pathways for ERbeta activation in PC cells. Moreover, 3beta-Adiol induces the expression of E-cadherin, a protein known to be capable to reduce metastasis formation of breast cancer and PC cells. The inhibitory effects of 3beta-Adiol on PC cell migration is counteracted by siRNA against E-cadherin. The present data demonstrated that 1) Testosterone may exert an estrogenic effects downstream in the catabolic process present in the prostate; 2) the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) inhihits cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against PC invasion and metastasis. These results may help to explain some clinical observations which reported that alterations in gene coding for 3beta-HSDs (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary PC.
Vittoria Guerini - One of the best experts on this subject based on the ideXlab platform.
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the androgen Derivative 5α androstane 3β 17β diol inhibits prostate cancer cell migration through activation of the estrogen receptor β subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Eugenia Scaccianoce, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5α-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor–independent mechanism. We have shown that the dihydroTestosterone metabolite 5α-androstane-3β,17β-diol (3β-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor β (ERβ), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERβ signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERβ activation in prostate cancer cells. Moreover, 3β-Adiol, through ERβ, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3β-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that ( a ) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and ( b ) that the estrogenic effect of Testosterone Derivatives (ERβ-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3β-hydroxysteroid dehydrogenases (the enzymes responsible for 3β-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol inhibits prostate cancer cell migration through activation of the estrogen receptor beta subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Benita S Katzenellenbogen, Eugenia Scaccianoce, Paolo Martini, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5alpha-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor-independent mechanism. We have shown that the dihydroTestosterone metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor beta (ERbeta), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERbeta signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERbeta activation in prostate cancer cells. Moreover, 3beta-Adiol, through ERbeta, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3beta-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that (a) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and (b) that the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3beta-hydroxysteroid dehydrogenases (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol 3beta adiol inhibits migration of prostate cancer cell by activation of the estrogen receptor beta
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Marcella Motta, Angelo PolettiAbstract:297 In earlier stages, prostate cancer (PC) depends on androgens and may be reduced with androgen blockade. Androgen-ablation therapy often induces androgen-independent PC, characterized by an increased invasiveness. We have found that the the Testosterone Derivative, dihydroTestosterone inhibits cell migration with an androgen receptor (AR)-independent mechanism. This effect has been linked to its metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind AR, but interact with the estrogen receptor beta (ERbeta). 3beta-Adiol inhibits cell migration of PC through the activation of the ERbeta signalling, while estradiol is not active, suggesting the existence of different pathways for ERbeta activation in PC cells. Moreover, 3beta-Adiol induces the expression of E-cadherin, a protein known to be capable to reduce metastasis formation of breast cancer and PC cells. The inhibitory effects of 3beta-Adiol on PC cell migration is counteracted by siRNA against E-cadherin. The present data demonstrated that 1) Testosterone may exert an estrogenic effects downstream in the catabolic process present in the prostate; 2) the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) inhihits cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against PC invasion and metastasis. These results may help to explain some clinical observations which reported that alterations in gene coding for 3beta-HSDs (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary PC.
Fabio Facchinetti - One of the best experts on this subject based on the ideXlab platform.
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The paradigm of norgestimate: a third-generation Testosterone-Derivative progestin with a peripheral anti-androgenic activity and the lowest risk of venous thromboembolism
Expert review of clinical pharmacology, 2021Co-Authors: Giovanni Grandi, Maria Chiara Del Savio, Fabio FacchinettiAbstract:Norgestimate (NGM) is a Testosterone Derivative with peculiar receptor activities. This is a narrative review of the available data on the pharmacotherapy of NGM in combined hormonal contraceptives...
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The paradigm of norgestimate: a third-generation Testosterone-Derivative progestin with a peripheral anti-androgenic activity and the lowest risk of venous thromboembolism.
Expert review of clinical pharmacology, 2021Co-Authors: Giovanni Grandi, Maria Chiara Del Savio, Fabio FacchinettiAbstract:Norgestimate (NGM) represents an interesting progestin, as it is a Testosterone Derivative with peculiar receptor activities. This is a narrative review of the available data on the pharmacotherapy of NGM in combined hormonal contraceptives (CHCs) in terms of contraceptive efficacy, venous thromboembolism (VTE) risk, safety, tolerability and bleeding patterns. A comprehensive literature review was conducted in August 2020 using PubMed with the keyword "norgestimate". NGM shows a mild estrogenic activity associated with anti-mineralocorticoid and anti-androgenic properties, largely responsible for the cardiovascular safety profile. The anti-androgenic property depends on the androgen receptor (AR) nuclear translocation (AR trafficking and its subnuclear distribution), the inhibition of 5α-reductase activity (it possesses higher activity compared to other available progestins), and the increase on sexual hormone binding globulin (SHBG) levels if combined with an estrogenic counterpart. NGM is one of the molecules that best modulate the power of ethinyl-estradiol on the thromboembolic risk, being associated with the lowest VTE risk between different CHCs. NGM has the advantage of retaining peripheral anti-androgenic activity, demonstrated by the impact on lipid and glucose metabolism, and it should be preferred if compared with other similar progestins of the same class of risk which are much more androgenic, such as levonorgestrel.
Benita S Katzenellenbogen - One of the best experts on this subject based on the ideXlab platform.
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the androgen Derivative 5α androstane 3β 17β diol inhibits prostate cancer cell migration through activation of the estrogen receptor β subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Eugenia Scaccianoce, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5α-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor–independent mechanism. We have shown that the dihydroTestosterone metabolite 5α-androstane-3β,17β-diol (3β-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor β (ERβ), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERβ signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERβ activation in prostate cancer cells. Moreover, 3β-Adiol, through ERβ, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3β-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that ( a ) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and ( b ) that the estrogenic effect of Testosterone Derivatives (ERβ-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3β-hydroxysteroid dehydrogenases (the enzymes responsible for 3β-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol inhibits prostate cancer cell migration through activation of the estrogen receptor beta subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Benita S Katzenellenbogen, Eugenia Scaccianoce, Paolo Martini, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5alpha-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor-independent mechanism. We have shown that the dihydroTestosterone metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor beta (ERbeta), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERbeta signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERbeta activation in prostate cancer cells. Moreover, 3beta-Adiol, through ERbeta, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3beta-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that (a) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and (b) that the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3beta-hydroxysteroid dehydrogenases (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol 3beta adiol inhibits migration of prostate cancer cell by activation of the estrogen receptor beta
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Marcella Motta, Angelo PolettiAbstract:297 In earlier stages, prostate cancer (PC) depends on androgens and may be reduced with androgen blockade. Androgen-ablation therapy often induces androgen-independent PC, characterized by an increased invasiveness. We have found that the the Testosterone Derivative, dihydroTestosterone inhibits cell migration with an androgen receptor (AR)-independent mechanism. This effect has been linked to its metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind AR, but interact with the estrogen receptor beta (ERbeta). 3beta-Adiol inhibits cell migration of PC through the activation of the ERbeta signalling, while estradiol is not active, suggesting the existence of different pathways for ERbeta activation in PC cells. Moreover, 3beta-Adiol induces the expression of E-cadherin, a protein known to be capable to reduce metastasis formation of breast cancer and PC cells. The inhibitory effects of 3beta-Adiol on PC cell migration is counteracted by siRNA against E-cadherin. The present data demonstrated that 1) Testosterone may exert an estrogenic effects downstream in the catabolic process present in the prostate; 2) the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) inhihits cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against PC invasion and metastasis. These results may help to explain some clinical observations which reported that alterations in gene coding for 3beta-HSDs (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary PC.
Adriana Maggi - One of the best experts on this subject based on the ideXlab platform.
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the androgen Derivative 5α androstane 3β 17β diol inhibits prostate cancer cell migration through activation of the estrogen receptor β subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Eugenia Scaccianoce, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5α-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor–independent mechanism. We have shown that the dihydroTestosterone metabolite 5α-androstane-3β,17β-diol (3β-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor β (ERβ), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERβ signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERβ activation in prostate cancer cells. Moreover, 3β-Adiol, through ERβ, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3β-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that ( a ) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and ( b ) that the estrogenic effect of Testosterone Derivatives (ERβ-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3β-hydroxysteroid dehydrogenases (the enzymes responsible for 3β-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol inhibits prostate cancer cell migration through activation of the estrogen receptor beta subtype
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Benita S Katzenellenbogen, Eugenia Scaccianoce, Paolo Martini, L Martini, Marcella MottaAbstract:Prostate cancer growth depends, in its earlier stages, on androgens and is usually pharmacologically modulated with androgen blockade. However, androgen-ablation therapy may generate androgen-independent prostate cancer, often characterized by an increased invasiveness. We have found that the 5alpha-reduced Testosterone Derivative, dihydroTestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor-independent mechanism. We have shown that the dihydroTestosterone metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind androgen receptors, but efficiently binds the estrogen receptor beta (ERbeta), exerts a potent inhibition of prostate cancer cell migration through the activation of the ERbeta signaling. Very surprisingly, estradiol is not active, suggesting the existence of different pathways for ERbeta activation in prostate cancer cells. Moreover, 3beta-Adiol, through ERbeta, induces the expression of E-cadherin, a protein known to be capable of blocking metastasis formation in breast and prostate cancer cells. The inhibitory effects of 3beta-Adiol on prostate cancer cell migration is counteracted by short interfering RNA against E-cadherin. Altogether, the data showed that (a) circulating Testosterone may act with estrogenic effects downstream in the catabolic process present in the prostate, and (b) that the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) results in the inhibition of cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against prostate cancer invasion and metastasis. These results also shed some light on clinical observations suggesting that alterations in genes coding for 3beta-hydroxysteroid dehydrogenases (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary prostate cancer.
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the androgen Derivative 5alpha androstane 3beta 17beta diol 3beta adiol inhibits migration of prostate cancer cell by activation of the estrogen receptor beta
Cancer Research, 2005Co-Authors: Vittoria Guerini, Daniela Sau, Paola Rusmini, Paolo Ciana, Adriana Maggi, Paolo G V Martini, Benita S Katzenellenbogen, Marcella Motta, Angelo PolettiAbstract:297 In earlier stages, prostate cancer (PC) depends on androgens and may be reduced with androgen blockade. Androgen-ablation therapy often induces androgen-independent PC, characterized by an increased invasiveness. We have found that the the Testosterone Derivative, dihydroTestosterone inhibits cell migration with an androgen receptor (AR)-independent mechanism. This effect has been linked to its metabolite 5alpha-androstane-3beta,17beta-diol (3beta-Adiol), a steroid which does not bind AR, but interact with the estrogen receptor beta (ERbeta). 3beta-Adiol inhibits cell migration of PC through the activation of the ERbeta signalling, while estradiol is not active, suggesting the existence of different pathways for ERbeta activation in PC cells. Moreover, 3beta-Adiol induces the expression of E-cadherin, a protein known to be capable to reduce metastasis formation of breast cancer and PC cells. The inhibitory effects of 3beta-Adiol on PC cell migration is counteracted by siRNA against E-cadherin. The present data demonstrated that 1) Testosterone may exert an estrogenic effects downstream in the catabolic process present in the prostate; 2) the estrogenic effect of Testosterone Derivatives (ERbeta-dependent) inhihits cell migration, although it is apparently different from that linked to estradiol on the same receptor and may be protective against PC invasion and metastasis. These results may help to explain some clinical observations which reported that alterations in gene coding for 3beta-HSDs (the enzymes responsible for 3beta-Adiol formation) are strongly correlated with hereditary PC.