ArticleMolecular endocrinology (Baltimore, Md.)2009
Repression of Runx2 by androgen receptor (AR) in osteoblasts and prostate cancer cells: AR binds Runx2 and abrogates its recruitment to DNA.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 68 citations in OpenAlex.
- Ufl1-Mediated UFMylation Sustains Amelogenesis by Stabilizing RUNX2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
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- Probable Treatment Targets for Diabetic Retinopathy Based on an Integrated Proteomic and Genomic Analysis.Translational vision science & technology · 2023Article
- CRISPR screens reveal genetic determinants of PARP inhibitor sensitivity and resistance in prostate cancer.Nature communications · 2023Article
- Molecular Evolution of Ecological Specialisation: Genomic Insights from the Diversification of Murine Rodents.Genome biology and evolution · 2021Article
- Prostate cancer racial, socioeconomic, geographic disparities: targeting the genomic landscape and splicing events in search for diagnostic, prognostic and therapeutic targets.American journal of cancer research · 2021Review
- Androgen receptor signaling regulates the transcriptome of prostate cancer cells by modulating global alternative splicing.Oncogene · 2020Article
- Characterization of CD44 intracellular domain interaction with RUNX2 in PC3 human prostate cancer cells.Cell communication and signaling : CCS · 2019Article
- Targeting the MIF/CXCR7/AKT Signaling Pathway in Castration-Resistant Prostate Cancer.Molecular cancer research : MCR · 2019Article
- Estrogens and selective estrogen receptor modulators differentially antagonize Runx2 in ST2 mesenchymal progenitor cells.The Journal of steroid biochemistry and molecular biology · 2018Article
- Estrogens and androgens inhibit association of RANKL with the pre-osteoblast membrane through post-translational mechanisms.Journal of cellular physiology · 2017Article
- Relationship between RUNX1 and AXIN1 in ER-negative versus ER-positive Breast Cancer.Cell cycle (Georgetown, Tex.) · 2017Article
- Glucocorticoids Hijack Runx2 to Stimulate Wif1 for Suppression of Osteoblast Growth and Differentiation.Journal of cellular physiology · 2017Article
- Inhibition of androgen receptor by decoy molecules delays progression to castration-recurrent prostate cancer.PloS one · 2017Article
- Glucocorticoid-Induced Osteoporosis.Advances in experimental medicine and biology · 2015Review
- Sex steroid actions in male bone.Endocrine reviews · 2014Review
- Association of polyalanine and polyglutamine coiled coils mediates expansion disease-related protein aggregation and dysfunction.Human molecular genetics · 2014Article
- Differential effects of RUNX2 on the androgen receptor in prostate cancer: synergistic stimulation of a gene set exemplified by SNAI2 and subsequent invasiveness.Cancer research · 2014Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Runx2 and androgen receptor (AR) are master transcription factors with pivotal roles in bone metabolism and prostate cancer (PCa). We dissected AR-mediated repression of Runx2 in dihydrotestosterone (DHT)-treated osteoblastic and PCa cells using reporter assays and endogenous Runx2 target genes. Repression required DHT, but not AR's transactivation function, and was associated with nuclear colocalization of the two proteins. Runx2 and AR coimmunoprecipitated and interacted directly in glutathione-S-transferase pull-down assays. Interaction was ionic in nature. Intact AR DNA-binding domain (DBD) was necessary and sufficient for both interaction with Runx2 and its repression. Runx2 sequences required for interaction were the C-terminal 132 amino acid residues together with the Runt DBD. Runx2 DNA binding was abrogated by endogenous AR in chromatin immunoprecipitation assays and by recombinant AR-DBD in gel shift assays. Furthermore, AR caused increased nuclear mobility of Runx2 as indicated by faster fluorescence recovery after photobleaching. Thus, AR binds Runx2 and abrogates its binding to DNA and possibly to other nuclear components. Clinical relevance of our results was suggested by an inverse correlation between expression of AR-responsive prostate-specific antigen and osteocalcin genes in PCa biopsies. Given the tumor suppressor properties of Runx2, its repression by AR may constitute a mechanism of hormone carcinogenesis. Attenuation of Runx2 by AR in osteoblasts may play a role in skeletal metabolism: the bone-sparing effect of androgens is attributable, in part, to keeping Runx2 activity in check and preventing high-turnover bone disease such as seen after castration and in transgenic mice overexpressing Runx2 in osteoblasts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.