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Department of Medicine, University of California, Los Angeles, California, USA
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Cholesterol and sex steroid hormones including androgens and estrogens play a critical role in the development and progression of urological diseases such as prostate cancer. This disease remains the most commonly diagnosed malignant tumor in men and is the leading cause of death from different cancers. Attempts to understand the role of cholesterol and steroid metabolism in urological diseases have been ongoing for many years, but despite this, our mechanistic and translational understanding remains elusive. In order to further evaluate the problem, we have taken an interest in metabolomics; a discipline dedicated to the systematic study of biologically active metabolites in cells, tissues, hair and biofluids. Recently, we provided evidence that a quantitative measurement of cholesterol and sex steroid metabolites can be successfully achieved using hair of human and mouse models. The overall goal of this short review article is to introduce current metabolomic technologies for the quantitative biomarker assay development and also to provide new insight into understanding the underlying mechanisms that trigger the pathological condition. Furthermore, this review will place a particular emphasis on how to prepare biospecimens (e.g., hair fiber), quantify molecular profiles and assess their clinical significance in various urological diseases.
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
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Prostate cancer (PCa) metastasis to bone is lethal and there is no adequate animal model for studying the mechanisms underlying the metastatic process. Here, we report that receptor activator of NF-κB ligand (RANKL) expressed by PCa cells consistently induced colonization or metastasis to bone in animal models. RANK-mediated signaling established a premetastatic niche through a feed-forward loop, involving the induction of RANKL and c-Met, but repression of androgen receptor (AR) expression and AR signaling pathways. Site-directed mutagenesis and transcription factor (TF) deletion/interference assays identified common TF complexes, c-Myc/Max, and AP4 as critical regulatory nodes. RANKL–RANK signaling activated a number of master regulator TFs that control the epithelial-to-mesenchymal transition (Twist1, Slug, Zeb1, and Zeb2), stem cell properties (Sox2, Myc, Oct3/4, and Nanog), neuroendocrine differentiation (Sox9, HIF1α, and FoxA2), and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1α, and Runx2). Abrogating RANK or its downstream c-Myc/Max or c-Met signaling network minimized or abolished skeletal metastasis in mice. RANKL-expressing LNCaP cells recruited and induced neighboring non metastatic LNCaP cells to express RANKL, c-Met/activated c-Met, while downregulating AR expression. These initially non-metastatic cells, once retrieved from the tumors, acquired the potential to colonize and grow in bone. These findings identify a novel mechanism of tumor growth in bone that involves tumor cell reprogramming via RANK–RANKL signaling, as well as a form of signal amplification that mediates recruitment and stable transformation of non-metastatic bystander dormant cells.
