ArticleJournal of cellular biochemistry2012
Recruitment of coregulator G9a by Runx2 for selective enhancement or suppression of transcription.
Article in Journal of cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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
32 citing papers in PubMed, 54 citations in OpenAlex.
- Histone methyltransferase G9a drives vascular smooth muscle cell proliferation and intimal hyperplasia in mice.Acta pharmacologica Sinica · 2026Article
- G9a controls plasma cell differentiation through FOXO1 and ETS1 binding site regulatory networks.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Role and mechanisms of histone methylation in osteogenic/odontogenic differentiation of dental mesenchymal stem cells.International journal of oral science · 2025Review
- Histone-modifying enzymes as drivers and therapeutic targets in androgen-resistant prostate cancer.Frontiers in endocrinology · 2025Review
- The histone H3K9 methyltransferase G9a regulates tendon formation during development.Scientific reports · 2024Article
- Article
- Discovery of the First-in-Class G9a/GLP PROTAC Degrader.Journal of medicinal chemistry · 2024Article
- Discovery of the First-in-class G9a/GLP PROTAC Degrader.bioRxiv : the preprint server for biology · 2024Article
- Transcriptional coactivation by EHMT2 restricts glucocorticoid-induced insulin resistance in a study with male mice.Nature communications · 2023Article
- Review
- Cellular specificity of androgen receptor, coregulators, and pioneer factors in prostate cancer.Endocrine oncology (Bristol, England) · 2022Review
- Structure, Activity, and Function of the Protein Lysine Methyltransferase G9a.Life (Basel, Switzerland) · 2021Review
- Histone Methyltransferase G9a Promotes the Development of Renal Cancer through Epigenetic Silencing of Tumor Suppressor Gene SPINK5.Oxidative medicine and cellular longevity · 2021Article
- Article
- Expression of the ectodomain-releasing protease ADAM17 is directly regulated by the osteosarcoma and bone-related transcription factor RUNX2.Journal of cellular biochemistry · 2018Article
- Nuclear receptors in cancer - uncovering new and evolving roles through genomic analysis.Nature reviews. Genetics · 2018Review
- A post-translational modification switch controls coactivator function of histone methyltransferases G9a and GLP.EMBO reports · 2017Article
- G9A promotes tumor cell growth and invasion by silencing CASP1 in non-small-cell lung cancer cells.Cell death & disease · 2017Article
- Article
- The expanding role of the Ehmt2/G9a complex in neurodevelopment.Neurogenesis (Austin, Tex.) · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Runx2, best known for its role in regulating osteoblast-specific gene expression, also plays an increasingly recognized role in prostate and breast cancer metastasis. Using the C4-2B/Rx2(dox) prostate cancer cell line that conditionally expressed Runx2 in response to doxycycline treatment, we identified and characterized G9a, a histone methyltransferase, as a novel regulator for Runx2 activity. G9a function was locus-dependent. Whereas depletion of G9a reduced expression of many Runx2 target genes, including MMP9, CSF2, SDF1, and CST7, expression of others, such as MMP13 and PIP, was enhanced. Physical association between G9a and Runx2 was indicated by co-immunoprecipitation, GST-pulldown, immunofluorescence, and fluorescence recovery after photobleaching (FRAP) assays. Since G9a makes repressive histone methylation marks and is primarily known as a corepressor, we further investigated the mechanism by which G9a functioned as a positive regulator for Runx2 target genes. Transient reporter assays indicated that the histone methyltransferase activity of G9a was not required for transcriptional activation by Runx2. Chromatin immunoprecipitation assays for Runx2 and G9a showed that G9a was recruited to endogenous Runx2 binding sites. We conclude that a subset of cancer-related Runx2 target genes require recruitment of G9a for their expression, but do not depend on its histone methyltransferase activity.
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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.