Project description:Histone methyltransferases (HMTases), as chromatin modifiers, regulate the transcriptomic landscape in normal development as well in diseases such as cancer. Here, we molecularly order two HMTases, EZH2 and MMSET that have established genetic links to oncogenesis. EZH2, which mediates histone H3K27 trimethylation and is associated with gene silencing, was shown to be coordinately expressed and function upstream of MMSET, which mediates H3K36 dimethylation and is associated with active transcription. We found that the EZH2-MMSET HMTase axis is coordinated by a microRNA network and that the oncogenic functions of EZH2 require MMSET activity. Together, these results suggest that the EZH2-MMSET HMTase axis coordinately functions as a master regulator of transcriptional repression, activation, and oncogenesis and may represent an attractive therapeutic target in cancer. Examination of H3K36me2 mark in control and stable EZH2 knockdown cells
Project description:Dicer and Argonaute2 (Ago2) gene is involving in microRNA (miRNA) maturation. Knockdown of these genes has great impact on miRNA expression profiles. We used microarrays to detail the miRNA expression profiles in Dicer- and Ago2-knockdown HeLa cells and demonstarted that the significant difference between Ago2-knockdown and Dicer- and Ago2-co-knockdown HeLa cells were not found.
Project description:Knockdown of EZH2 in colorectal cancer cells by lentivirus-mediated shRNA, and use total RNA for sequencing analysis after determining the efficiency of EZH2 knockdown in order to analyze the gene expression affected by EZH2.
Project description:EZH2, the catalytic component of the Polycomb repressive complex 2 (PRC2), silences gene transcription by methylating histone H3 at lysine 27. Recently we identified ZRANB1 as the EZH2 deubiquitinase. ZRANB1 binds, deubiquitinates, and stabilizes EZH2. To determine whether ZRANB1 is a functional regulator of EZH2, we performed RNA-Seq analysis to compare the effect of ZRANB1 knockdown or EZH2 knockdown on global gene expression.
Project description:The findings indicate that EZH2 may act as a important therapeutic target for treatment of EAC. Furherly, EZH2 knockdown couldinduce G2/M phase arrest and resulted in cell proliferation inhibition. To further investigate how EZH2 overexpression impacted cell proliferation of EAC, Microarray gene expression profiling was performed on ISK cell line with or without EZH2 knockdown.
Project description:To identify genes whose expression was suppressed by EZH2, we performed gene expression microarray analysis in control and EZH2 knockdown human SKOV3 EOC cells. Two individual short hairpin RNAs to the human EZH2 gene (shEZH2) were used to limit potential off-target effects.
