Nonsteroidal Anti-inflammatory Drug-activated Gene (NAG-1/GDF15) Expression Is Increased by the Histone Deacetylase Inhibitor Trichostatin A *
Journal of Biological Chemistry, ISSN: 0021-9258, Vol: 283, Issue: 48, Page: 33129-33137
2008
- 42Citations
- 32Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations42
- Citation Indexes42
- 42
- CrossRef35
- Captures32
- Readers32
- 32
Article Description
Nonsteroidal anti-inflammatory drug-activated gene ( NAG-1 ) is a putative tumor suppressor whose expression can be increased by drug treatment. Glioblastoma is the most common central nervous system tumor, is associated with high morbidity and mortality, and responds poorly to surgical, chemical, and radiation therapy. The histone deacetylase inhibitors are under current consideration as therapeutic agents in treating glioblastoma. We investigated whether trichostatin A (TSA) would alter the expression of NAG-1 in glioblastoma cells. The DNA demethylating agent 5-aza-dC did not increase NAG-1 expression, but TSA up-regulated NAG-1 expression and acted synergistically with 5-aza-dC to induce NAG-1 expression. TSA indirectly increases NAG-1 promoter activity and increases NAG-1 mRNA and protein expression in the T98G human glioblastoma cell line. TSA also increases the expression of transcription factors Sp-1 and Egr-1. Small interfering RNA experiments link NAG-1 expression to apoptosis induced by TSA. Reporter gene assays, specific inhibition by small interfering RNA transfections, and chromatin immunoprecipitation assays indicate that Egr-1 and Sp-1 mediate TSA-induced NAG-1 expression. TSA also increases the stability of NAG-1 mRNA. TSA-induced NAG-1 expression involves multiple mechanisms at the transcriptional and post-transcriptional levels.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0021925820634573; http://dx.doi.org/10.1074/jbc.m805248200; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=57749089765&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/18801729; http://www.jbc.org/lookup/doi/10.1074/jbc.M805248200; https://syndication.highwire.org/content/doi/10.1074/jbc.M805248200; https://linkinghub.elsevier.com/retrieve/pii/S0021925820634573; https://dx.doi.org/10.1074/jbc.m805248200
American Society for Biochemistry & Molecular Biology (ASBMB)
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