Cancer Cell Biology
RBP2-H1/JARID1B is a transcriptional regulator with a tumor suppressive potential in melanoma cells
Article first published online: 31 OCT 2007
Copyright © 2007 Wiley-Liss, Inc.
International Journal of Cancer
Volume 122, Issue 5, pages 1047–1057, 1 March 2008
How to Cite
Roesch, A., Mueller, A. M., Stempfl, T., Moehle, C., Landthaler, M. and Vogt, T. (2008), RBP2-H1/JARID1B is a transcriptional regulator with a tumor suppressive potential in melanoma cells. Int. J. Cancer, 122: 1047–1057. doi: 10.1002/ijc.23211
- Issue published online: 24 DEC 2007
- Article first published online: 31 OCT 2007
- Manuscript Accepted: 7 SEP 2007
- Manuscript Received: 13 JUL 2007
- German Dermatologic Society (DDG)
- gene expression;
- retinoblastoma protein binding protein;
The RBP2-H1/JARID1B nuclear protein belongs to the ARID family of DNA-binding proteins and is a potential tumor suppressor that is lost during melanoma development. As we have recently shown, one physiological function of RBP2-H1/JARID1B is to exert cell cycle control via maintenance of active retinoblastoma protein. We now add new evidence that RBP2-H1/JARID1B can also directly regulate gene transcription in a reporter assay system, either alone or as part of a multimolecular complex together with the developmental transcription factors FOXG1b and PAX9. In melanoma cells, chromatin immunoprecipitation combined with promoter chip analysis (ChIP-on-chip) suggests a direct binding of re-expressed RBP2-H1/JARID1B to a multitude of human regulatory chromosomal elements (promoters, enhancers and introns). Among those, a set of 23 genes, including the melanoma relevant genes CDK6 and JAG-1 could be confirmed by cDNA microarray analyses to be differentially expressed after RBP2-H1/JARID1B re-expression. In contrast, in nonmelanoma HEK 293 cells, RBP2-H1/JARID1B overexpression only evokes a minor transcriptional response in cDNA microarray analyses. Because the transcriptional regulation in melanoma cells is accompanied by an inhibition of proliferation, an increase in caspase activity and a partial cell cycle arrest in G1/0, our data support an anti-tumorigenic role of RBP2-H1/JARID1B in melanocytic cells. © 2007 Wiley-Liss, Inc.