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Lung cancer-associated JmjC domain protein mdig suppresses formation of tri-methyl lysine 9 of histone H3.

Authors
Lu-Y; Chang-Q; Zhang-Y; Beezhold-K; Rojanasakul-Y; Zhao-H; Castranova-V; Shi-X; Chen-F
Source
Cell Cycle 2009 Jul; 8(13):2101-2109
NIOSHTIC No.
20035649
Abstract
Lung cancer is the most common cancer worldwide, accounting for 1.3 million cancer deaths annually. Despite extensive studies over the past decade, the detailed mechanism about the initiation and development of the lung cancer is still elusive. In the present report, we showed that overexpression of mdig is a common feature of the non-small cell lung cancer. Gene silencing or overexpression of mdig revealed that mdig is involved in demethylation of tri-methyl lysine 9 on histone H3, leading to an increase in ribosomal RNA expression. The transcriptional regulation of ribosomal RNA gene by mdig is achieved through abrogating tri-methyl lysine 9 on histone H3 and enhancing RNA polymerase I occupancy in the promoter region of the ribosomal RNA gene as demonstrated by chromatin immunoprecipitation. The pronounced expression of mdig in lung cancer tissues but not normal lung tissues, thus, suggests that mdig possesses oncogenic property through antagonizing tri-methyl lysine 9 on histone H3 and promoting ribosomal RNA synthesis.
Keywords
Lung-cancer; Lung-disease; Lung-disorders; Pulmonary-system-disorders; Pulmonary-cancer; Respiratory-system-disorders; Respiratory-neoplasms; Cancer; Author Keywords: mdig gene; histone demethylation; lung cancer; mineral dust; H3K9me3
CODEN
CCEYAS
Publication Date
20090701
Document Type
Journal Article
Email Address
lfd3@cdc.gov
Fiscal Year
2009
NTIS Accession No.
NTIS Price
Issue of Publication
13
ISSN
1538-4101
NIOSH Division
HELD
Priority Area
Manufacturing; Mining
Source Name
Cell Cycle
State
WV; KY
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