We found that lncRNA ZNFX1-AS1 is significantly upregulated in CRC, and the newly identified lncRNA ZNFX1-AS1-miR-144-EZH2 axis is involved in the regulation of CRC progression, which might be used as potential therapeutic targets for CRC patients.
Further investigation demonstrated that lncRNA BDNF-AS functioned as a tumour suppressor in CRC progression by suppressing GSK-3β expression through binding to EZH2 and H3K27me3 with the GSK-3β promoter, shedding light on the diagnosis and therapy for CRC.
Collectively, we concluded that MALAT1 functioned as a ceRNA to promote colorectal cancer development and EZH2 expression through sponging miR-363-3p <i>in vitro</i> and <i>in vivo</i>.
We found a weak expression of EZH2 in normal colon mucosa that increased in low grade, peaked in high grade intraepithelial neoplasia, and decreased again in invasive CRC.
<b>Methods:</b> The expression levels of SNHG6, miR-26a, and enhancer of zeste homolog 2 (EZH2) mRNA were assessed by quantification real-time PCR in CRC tissues and cell lines.
In addition, O-GlcNAcylation and H3K27me3 modification in the miR-101 promoter region further inhibited the transcription of miR-101, resulting in the upregulation of OGT and EZH2 in metastatic CRC, thus forming a vicious cycle.
These results demonstrated that the hsa_circ_0071589/miR-600/EZH2 axis may play critical regulatory roles in the pathogenesis of CRC and may serve as a novel therapy target in CRC.
The aim was to evaluate serum levels of circulating cell-free nucleosomes (ccfn) containing a variety of epigenetic signals including 5-methylcytosine DNA, histone modifications H3K9Me3, H3K9Ac, H3S10PO4, H3K36Me3, H4K20Me3, H4PanAc and pH2AX, nucleosome variant H2AZ and nucleosome adducts with HMGB1 and EZH2 as well as ccfn per se, in addition to develop and evaluate predictor models based on the above mentioned ccfn and including serum levels of carcinoembryonic antigen (CEA), in early detection of colorectal cancer (CRC).
Additionally, methyl jasmonate increased the activation of caspase-3, inhibited the expression levels of enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and the Wnt/β-catenin pathway in human colorectal cancer.
Our data reveal that lncRNA XIST may promote tumor metastasis in CRC possibly through regulating the miR-137-EZH2 axis. lncRNA XIST may serve as a prognostic indicator for CRC progression.
Thus, we sought to examine the prognostic value of histone-modifying enzymes (EZH2, SETDB1 and LSD-1) and histone post-translational marks (H3K27me3 and H3K9me3) in CRC.
Furthermore, RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that lncRNA CRNDE could epigenetically suppress the expressions of dual-specificity phosphatase 5 (DUSP5) and CDKN1A by binding to EZH2 (the key components of Polycomb repressive complex 2 (PRC2)), thus promoting CRC development.
EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in colorectal cancer, and this association suppressed the expression of E-cadherin.