Abstract
Enhancer of zeste homolog 2 (EZH2) is the catalitic subunit of polycomb repressive complex 2 and mediates gene silencing. EZH2 is overexpressed in many cancers and correlates with poor prognosis. The role of the gene EZH2 in colorectal cancer survival is uncertainly, the aim of this study is clear this relationship. Relevant literaure was searched from electronic databases. A meta-analysis was performed with elegible studies which quantitatively evaluated the relationship between EZH2 overexpression and survival of patients with colorectal cancer. Survival data were aggregated and quantitatively analyzed. We performed a meta-analysis of 8 studies (n = 1059 patients) that evaluated the correlation between EZH2 overexpression and survival in patients with colorectal cancer. Combined hazard ratios suggested that EZH2 overexpression was associated with better prognosis of overall survival (OS) HR(hazard ratio) = 0.61 95% CI (0.38–0.84) We performed bias analysis according Egger and Begg,s test and we did not find publication bias. EZH2 overexpression indicates a better prognosis for colorectal cancer.
Highlights
Colorectal cancer (CRC) is one of the main causes of death in industrialized countries, coming in third place for incidence and fourth for mortality in the world as a whole[1]
It is believed that the Enhancer of zeste homolog 2 (EZH2) protein participates in the transcriptional repression of genes through various mechanisms, such as trimethylation of the residue of lysine 27 of histone H3 (H3mek27), or methylation of the CpG islands It operates as a platform recruiting other enzymes involved in gene silencing, like histone de-acetylases (HDACs)[7,8] and methyltransferases (DNMT1, DNMT3A, and DNMT3b)[9]
A good number of studies suggest that the over-expression of EZH2 may have a prognostic value in some types of cancer, and it has been associated with a worse prognosis and survival rate in breast and prostate tumours[7,14,15,26]
Summary
Colorectal cancer (CRC) is one of the main causes of death in industrialized countries, coming in third place for incidence and fourth for mortality in the world as a whole[1]. Colorectal cancer develops from the progressive accumulation of molecular events, like somatic mutations in oncogenes, or epigenetic mechanisms such as methylation of DNA or post-transcriptional modification of histones[2]. One of the mechanisms that regulate histone epigenetic modification is mediated by the polycomb repressive complexes (PcG). It is believed that the EZH2 protein participates in the transcriptional repression of genes through various mechanisms, such as trimethylation of the residue of lysine 27 of histone H3 (H3mek27), or methylation of the CpG islands It operates as a platform recruiting other enzymes involved in gene silencing, like histone de-acetylases (HDACs)[7,8] and methyltransferases (DNMT1, DNMT3A, and DNMT3b)[9]. A limited number of studies focus on the relationship between the expression de EZH2 and overall and disease free survival or with responses to treatment
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