Steroid Synthesis Activates Androgen Receptor in Castration-Resistant Prostate Cancer and Is Upregulated by Treatment with CYP17A1 Inhibitors Article Swipe

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Changmeng Cai , Sen Chen , Patrick Ng , Glenn J. Bubley , Peter S. Nelson , Elahe A. Mostaghel , Brett T. Marck , Alvin M. Matsumoto , Nicholas I. Simon , Hongyun Wang , Shaoyong Chen , Steven P. Balk ·

YOU? · · 2023 · Open Access · · DOI: https://doi.org/10.1158/0008-5472.c.6502257.v1

Relapse of castration-resistant prostate cancer (CRPC) that occurs after androgen deprivation therapy of primary prostate cancer can be mediated by reactivation of the androgen receptor (AR). One important mechanism mediating this AR reactivation is intratumoral conversion of the weak adrenal androgens DHEA and androstenedione into the AR ligands testosterone and dihydrotestosterone. DHEA and androstenedione are synthesized by the adrenals through the sequential actions of the cytochrome P450 enzymes CYP11A1 and CYP17A1, so that CYP17A1 inhibitors such as abiraterone are effective therapies for CRPC. However, the significance of intratumoral CYP17A1 and de novo androgen synthesis from cholesterol in CRPC, and the mechanisms contributing to CYP17A1 inhibitor resistance/relapse, remain to be determined. We report that AR activity in castration-resistant VCaP tumor xenografts can be restored through CYP17A1-dependent de novo androgen synthesis, and that abiraterone treatment of these xenografts imposes selective pressure for increased intratumoral expression of CYP17A1, thereby generating a mechanism for development of resistance to CYP17A1 inhibitors. Supporting the clinical relevance of this mechanism, we found that intratumoral expression of CYP17A1 was markedly increased in tumor biopsies from CRPC patients after CYP17A1 inhibitor therapy. We further show that CRPC cells expressing a progesterone responsive T877A mutant AR are not CYP17A1 dependent, but that AR activity in these cells is still steroid dependent and mediated by upstream CYP11A1-dependent intraturmoral pregnenolone/progesterone synthesis. Together, our results indicate that CRPCs resistant to CYP17A1 inhibition may remain steroid dependent and therefore responsive to therapies that can further suppress de novo intratumoral steroid synthesis. Cancer Res; 71(20); 6503–13. ©2011 AACR.

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Prostate cancer CYP17A1 Downregulation and upregulation Androgen receptor Castration Androgen deprivation therapy Steroid Prostate Androgen Cancer research Medicine Endocrinology Internal medicine Cancer Chemistry Hormone Gene Biochemistry

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Type: preprint
Language: en
Landing Page: https://doi.org/10.1158/0008-5472.c.6502257.v1
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DOI: https://doi.org/10.1158/0008-5472.c.6502257.v1

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Title: Data from Intratumoral <i>De Novo</i> Steroid Synthesis Activates Androgen Receptor in Castration-Resistant Prostate Cancer and Is Upregulated by Treatment with CYP17A1 Inhibitors

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Publication year: 2023

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Publication date: 2023-03-30

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Authors: Changmeng Cai, Sen Chen, Patrick Ng, Glenn J. Bubley, Peter S. Nelson, Elahe A. Mostaghel, Brett T. Marck, Alvin M. Matsumoto, Nicholas I. Simon, Hongyun Wang, Shaoyong Chen, Steven P. Balk

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Concepts: Prostate cancer, CYP17A1, Downregulation and upregulation, Androgen receptor, Castration, Androgen deprivation therapy, Steroid, Prostate, Androgen, Cancer research, Medicine, Endocrinology, Internal medicine, Cancer, Chemistry, Hormone, Gene, Biochemistry

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abstract_inverted_index.mediating	29
abstract_inverted_index.relevance	159
abstract_inverted_index.resistant	225
abstract_inverted_index.selective	137
abstract_inverted_index.synthesis	93
abstract_inverted_index.therapies	80, 237
abstract_inverted_index.therefore	234
abstract_inverted_index.treatment	132
abstract_inverted_index.6503–13.	250
abstract_inverted_index.Supporting	156
abstract_inverted_index.conversion	35
abstract_inverted_index.cytochrome	65
abstract_inverted_index.dependent,	199
abstract_inverted_index.expressing	189
abstract_inverted_index.expression	142, 167
abstract_inverted_index.generating	146
abstract_inverted_index.inhibition	228
abstract_inverted_index.inhibitors	74
abstract_inverted_index.mechanism,	162
abstract_inverted_index.mechanisms	100
abstract_inverted_index.resistance	152
abstract_inverted_index.responsive	192, 235
abstract_inverted_index.sequential	61
abstract_inverted_index.synthesis,	128
abstract_inverted_index.synthesis.	218, 246
abstract_inverted_index.xenografts	119, 135
abstract_inverted_index.<i>de	90, 125, 242
abstract_inverted_index.abiraterone	77, 131
abstract_inverted_index.cholesterol	95
abstract_inverted_index.deprivation	10
abstract_inverted_index.determined.	109
abstract_inverted_index.development	150
abstract_inverted_index.inhibitors.	155
abstract_inverted_index.synthesized	55
abstract_inverted_index.contributing	101
abstract_inverted_index.intratumoral	34, 87, 141, 166, 244
abstract_inverted_index.progesterone	191
abstract_inverted_index.reactivation	20, 32
abstract_inverted_index.significance	85
abstract_inverted_index.testosterone	48
abstract_inverted_index.intraturmoral	216
abstract_inverted_index.novo</i>	91, 126, 243
abstract_inverted_index.<i>Cancer	247
abstract_inverted_index.androstenedione	43, 53
abstract_inverted_index.CYP11A1-dependent	215
abstract_inverted_index.CYP17A1-dependent	124
abstract_inverted_index.resistance/relapse,	105
abstract_inverted_index.castration-resistant	2, 116
abstract_inverted_index.dihydrotestosterone.	50
abstract_inverted_index.pregnenolone/progesterone	217
abstract_inverted_index.<div>Abstract<p>Relapse	0
abstract_inverted_index.AACR</i>.</p></div>	252
cited_by_percentile_year
countries_distinct_count	0
institutions_distinct_count	12
sustainable_development_goals[0].id	https://metadata.un.org/sdg/3
sustainable_development_goals[0].score	0.5899999737739563
sustainable_development_goals[0].display_name	Good health and well-being
citation_normalized_percentile.value	0.48628001
citation_normalized_percentile.is_in_top_1_percent	False
citation_normalized_percentile.is_in_top_10_percent	False