Silencing of the Mouse H-rev107 Gene Encoding a Class II Tumor Suppressor by CpG Methylation *
Journal of Biological Chemistry, ISSN: 0021-9258, Vol: 277, Issue: 34, Page: 30543-30550
2002
- 20Citations
- 16Captures
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Metrics Details
- Citations20
- Citation Indexes20
- 20
- CrossRef19
- Captures16
- Readers16
- 16
Article Description
H-rev107 is a tumor suppressor originally isolated in revertants of H- ras -transformed cell lines. The gene is ubiquitously expressed in normal tissues but down-regulated in primary carcinomas or in many cell lines derived from tumors, including WEHI 7.1 lymphoma cells. Here, we show that unlike in H-rev107 -expressing cells or tissues the 5′-end of H-rev107 containing a CpG-rich region of 421 bp is highly methylated in WEHI 7.1 lymphoma cells, correlating with silencing of this gene. Repression of H-rev107 transcription in these cells could be relieved by chemically induced hypomethylation with 5-aza-dC. In addition, upon in vitro methylation, expression of the luciferase reporter gene driven by the H-rev107 promoter decreased by 80% in WEHI 7.1 and 293 cells. Furthermore, co-transfection of the methyl-CpG binding proteins, MeCP2 and MBD2, inhibited H-rev107 promoter activity up to 70% in SL2 cells when the promoter was methylated. By chromatin immunoprecipitation assays, we observed in vivo binding of MeCP2 and MBD2 to the 5′-end of H-rev107 in WEHI 7.1 cells, which was reduced to undetectable levels upon 5-aza-dC treatment, concluding that MeCP2 and MBD2 might be involved in silencing the methylated H-rev107 gene in lymphoma cells and probably certain tumors.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0021925820701298; http://dx.doi.org/10.1074/jbc.m111891200; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0037163072&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/12055182; https://linkinghub.elsevier.com/retrieve/pii/S0021925820701298; http://www.jbc.org/lookup/doi/10.1074/jbc.M111891200; https://syndication.highwire.org/content/doi/10.1074/jbc.M111891200; https://dx.doi.org/10.1074/jbc.m111891200
Elsevier BV
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