Title | Histone demethylase Jumonji D3 (JMJD3) as a tumor suppressor by regulating p53 protein nuclear stabilization. |
Publication Type | Journal Article |
Year of Publication | 2012 |
Authors | Ene CI, Edwards L, Riddick G, Baysan M, Woolard K, Kotliarova S, Lai C, Belova G, Cam M, Walling J, Zhou M, Stevenson H, Kim HSug, Killian K, Veenstra T, Bailey R, Song H, Zhang W, Fine HA |
Journal | PLoS One |
Volume | 7 |
Issue | 12 |
Pagination | e51407 |
Date Published | 2012 |
ISSN | 1932-6203 |
Keywords | Animals, Blotting, Western, Cell Differentiation, Cell Transformation, Neoplastic, DNA Primers, Glioblastoma, Histones, Humans, Immunohistochemistry, Immunoprecipitation, Jumonji Domain-Containing Histone Demethylases, Luciferases, Mass Spectrometry, Mice, Mice, SCID, Neoplastic Stem Cells, Protein Stability, Real-Time Polymerase Chain Reaction, Tumor Suppressor Protein p53 |
Abstract | Histone methylation regulates normal stem cell fate decisions through a coordinated interplay between histone methyltransferases and demethylases at lineage specific genes. Malignant transformation is associated with aberrant accumulation of repressive histone modifications, such as polycomb mediated histone 3 lysine 27 (H3K27me3) resulting in a histone methylation mediated block to differentiation. The relevance, however, of histone demethylases in cancer remains less clear. We report that JMJD3, a H3K27me3 demethylase, is induced during differentiation of glioblastoma stem cells (GSCs), where it promotes a differentiation-like phenotype via chromatin dependent (INK4A/ARF locus activation) and chromatin independent (nuclear p53 protein stabilization) mechanisms. Our findings indicate that deregulation of JMJD3 may contribute to gliomagenesis via inhibition of the p53 pathway resulting in a block to terminal differentiation. |
DOI | 10.1371/journal.pone.0051407 |
Alternate Journal | PLoS ONE |
PubMed ID | 23236496 |
PubMed Central ID | PMC3517524 |
Grant List | / / Howard Hughes Medical Institute / United States |