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The JMJD6-H2A.X(Y39ph) axis promoted triple negative breast cance cell growth via the autophagy pathway.
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results indicate for the first time that JMJD6 plays an important role in the regulation of ADSCs proliferation and migration through the modulation of PDE1C expression.
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Consistent with its role in transcriptional activation, JMJD6 is required for estrogen/ERalpha-induced breast cancer cell growth and tumorigenesis, via modulation of recruitment of CARM1/MED12 co-activator complex.
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JMJD6 is a novel Stress Granule component that interacts with G3BP1 complexes, and its expression reduces G3BP1 monomethylation and asymmetric dimethylation at three Arg residues.
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JMJD6 regulates VHL gene expression in the human placenta. VHL downregulation in preeclampsia is dependent on decreased JMJD6 demethylase activity due to hypoxia and reduced Fe2+ bioavailability.
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In tumor samples but not normal breast tissue, the expression of JMJD6 linearly correlated with HOTAIR suggesting that JMJD6-mediated up-regulation may occur specifically in tumors.
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Results show that JMJD6 is up-regulated in melanoma, and high expression of JMJD6 protein is strongly correlated with advanced stages and aggressiveness of melanoma. It enhances the MAPK signaling through regulation of alternative splicing of PAK1 promoting multiple cellular processes including melanogenesis, proliferation, invasion, and angiogenesis in melanoma cells.
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High JMJD6 expression is associated with Neuroblastomas.
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miR-770 acted on a tumor suppressor by binding to the 3'UTR of JMJD6 and downregulated its expression in NSCLC cells; this study also demonstrated that JMJD6 played as an oncogene in NSCLC cells
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JMJD6 regulated a large set of alternative splicing events, and importantly, its regulated splicing events were significantly overlapped those controlled by U2AF65.
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AcK27-HOXB9 suppresses the transcription of its target gene Jumonji domain-containing protein 6 (JMJD6) by direct occupying the promoter of JMJD6 gene.
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These findings provide evidence that JMJD6 may play a role in regulating the production of sFLT-1 in the preeclamptic placenta. Decreased placental JMJD6 expression may be an important component to the pathophysiology of preeclampsia.
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Study identified a novel epigenetic mechanism showing how JMJD6 cooperates with Myc during oncogenic transformation. Combined high expression of Myc and JMJD6 confers a more aggressive phenotype in mouse and human tumors.
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Our studies identify JMJD6 as a molecular determinant of cancer stem cell phenotype
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Although JMJD6 displays anti-tumoral properties in cell lines, its expression in breast tumours may be a marker of poor prognosis, suggesting that its function could be altered in breast cancer
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The expression of JMJD6 was reduced in T lymphocytes in chronic hepatitis B.
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A novel role for JMJD6 as an oxygen sensor in the human placenta, and alterations in the JMJD6-VHL-HIF1A feedback loop may indirectly contribute to elevated HIF1A found in preeclampsia.
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JMJD6 is a potential biomarker for colon cancer aggressiveness and a potential target for colon cancer intervention.
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Study reports that a unique cohort of JMJD6 and Brd4 cobound distal enhancers, termed anti-pause enhancers, regulate promoter-proximal pause release of a large subset of transcription units via long-range interactions.
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The structure of Jmjd6 oligomers in vitro changes in the absence of the polyS domain, possibly reflecting the role of the polyS domain in nuclear/nucleolar shuttling of Jmjd6.
