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- aggregation classification "A1".
- aggregation creator B764282.
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- aggregation creator person.
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- aggregation date "2013".
- aggregation format "application/pdf".
- aggregation hasFormat 4250441.bibtex.
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- aggregation isPartOf urn:issn:0305-1048.
- aggregation language "eng".
- aggregation rights "I have retained and own the full copyright for this publication".
- aggregation subject "Biology and Life Sciences".
- aggregation title "MYCN and HDAC2 cooperate to repress miR-183 signaling in neuroblastoma".
- aggregation abstract "MYCN is a master regulator controlling many processes necessary for tumor cell survival. Here, we unravel a microRNA network that causes tumor suppressive effects in MYCN-amplified neuroblastoma cells. In profiling studies, histone deacetylase (HDAC) inhibitor treatment most strongly induced miR-183. Enforced miR-183 expression triggered apoptosis, and inhibited anchorage-independent colony formation in vitro and xenograft growth in mice. Furthermore, the mechanism of miR-183 induction was found to contribute to the cell death phenotype induced by HDAC inhibitors. Experiments to identify the HDAC(s) involved in miR-183 transcriptional regulation showed that HDAC2 depletion induced miR-183. HDAC2 overexpression reduced miR-183 levels and counteracted the induction caused by HDAC2 depletion or HDAC inhibitor treatment. MYCN was found to recruit HDAC2 in the same complexes to the miR-183 promoter, and HDAC2 depletion enhanced promoter-associated histone H4 pan-acetylation, suggesting epigenetic changes preceded transcriptional activation. These data reveal miR-183 tumor suppressive properties in neuroblastoma that are jointly repressed by MYCN and HDAC2, and suggest a novel way to bypass MYCN function.".
- aggregation authorList BK1133336.
- aggregation endPage "6033".
- aggregation issue "12".
- aggregation startPage "6018".
- aggregation volume "41".
- aggregation aggregates 4267241.
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