ArticleEndocrinology2014
Steroidogenic factor 1 promotes aggressive growth of castration-resistant prostate cancer cells by stimulating steroid synthesis and cell proliferation.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Clinicopathological significance of steroidogenic factor-1 expression in ovarian cancer versus ovarian sex cord stromal tumor.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Pooled it
- An extra-genital cell population contributes to urethra closure during mouse penis development.bioRxiv : the preprint server for biology · 2023Article
- Orphan nuclear receptors as regulators of intratumoral androgen biosynthesis in castration-resistant prostate cancer.Oncogene · 2021Review
- Steroidogenesis in Peripheral and Transition Zones of Human Prostate Cancer Tissue.International journal of molecular sciences · 2021Article
- Article
- Review
- Cholesterol signaling in single cells: lessons from STAR and sm-FISH.Journal of molecular endocrinology · 2018Review
- 17Journal of the Endocrine Society · 2018Article
- The Orphan Nuclear Receptor Liver Homolog Receptor-1 (Nr5a2) Regulates Ovarian Granulosa Cell Proliferation.Journal of the Endocrine Society · 2018Article
- Conditional deletion of ELL2 induces murine prostate intraepithelial neoplasia.The Journal of endocrinology · 2017Article
- SF-1 deficiency causes lipid accumulation in Leydig cells via suppression of STAR and CYP11A1.Endocrine · 2016Article
- miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110.Oncotarget · 2016Article
- Interplay among Drosophila transcription factors Ets21c, Fos and Ftz-F1 drives JNK-mediated tumor malignancy.Disease models & mechanisms · 2015Article
- CD147 expression predicts biochemical recurrence after prostatectomy independent of histologic and pathologic features.BMC cancer · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The dependence of prostate cancer on androgens provides a targeted means of treating advanced disease. Unfortunately, androgen deprivation therapies eventually become ineffective, leading to deadly castration-resistant prostate cancer (CRPC). One of many factors implicated in the transition to CRPC is the onset of de novo steroidogenesis. Although reactivation of steroid receptors likely plays a pivotal role in aggressive CRPC, little is understood regarding the mechanisms whereby prostate cancer cells initiate and maintain steroidogenesis. We hypothesize that steroidogenic factor 1 (SF1, NR5A1, AD4BP), a key regulator of steroidogenesis in normal endocrine tissues, is expressed in CRPC where it stimulates aberrant steroidogenesis and fuels aggressive growth. Notably, SF1 is not expressed in normal prostate tissue. Our results indicated that SF1 was absent in benign cells but present in aggressive prostate cancer cell lines. Introduction of ectopic SF1 expression in benign human prostate epithelial cells (BPH-1) stimulated increased steroidogenic enzyme expression, steroid synthesis, and cell proliferation. In contrast, data from an aggressive human prostate cancer cell line (BCaPT10) demonstrated that SF1 was required for steroid-mediated cell growth because BCaPT10 cell growth was diminished by abiraterone treatment and short hairpin RNA-mediated knockdown of SF1 (shSF1). SF1-depleted cells also exhibited defective centrosome homeostasis. Finally, whereas xenograft experiments in castrated hosts with BCaPT10 control transplants grew large, invasive tumors, BCaPT10-shSF1 knockdown transplants failed to grow. Therefore, we conclude that SF1 stimulates steroid accumulation and controls centrosome homeostasis to mediate aggressive prostate cancer cell growth within a castrate environment. These findings present a new molecular mechanism and therapeutic target for deadly CRPC.
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