Abstract
Various studies examined the relationship between EZH2 overexpression with the clinical outcome in patients with non-small cell lung cancer (NSCLC), but yielded inconsistent results. Electronic databases updated to Dec 2014 were searched to find relevant studies. A meta-analysis was conducted with eligible studies which quantitatively evaluated the relationship between EZH2 overexpression and survival of patients with NSCLC Survival data were aggregated and quantitatively analyzed. We performed a meta-analysis of 10 studies (n = 1,695 patients) that evaluated the correlation between EZH2 overexpression and survival in patients with lung cancer. Combined hazard ratios suggested that EZH2 overexpression was associated with poor prognosis of overall survival (OS) (HR = 1.68, 95% CI: 1.42–1.93) in patients with lung cancer. In the stratified analysis, significantly risks were found among Asians (HR = 1.33, 95% CI: 1.62–1.70), lung adenocarcinoma patients (HR = 1.75, 95% CI: 1.38–2.52, in stage I NSCLC patients (HR = 2.51, 95% CI: 1.23–3.79), but not among Caucasians. EZH2 overexpression indicates a poor prognosis for patients with NSCLC, this effect appears also significant when the analysis is restricted in Asian population, lung AC and stage I patients, but not among Caucasians.
Highlights
Enhancer of zeste homolog 2 (EZH2) is a key component of the polycomb repressive complex 2, which possesses histone methyltransferase activity and mediates gene silencing through posttranslational histone modifications[6]
The studies were conducted in 3 countries
EZH2 is the catalytic subunit of PRC2, which catalyses the addition of methyl groups to lysine 27 on histone H3 (H3K27) in the promoters of target genes, leading to repression of gene transcription[27,28]
Summary
Enhancer of zeste homolog 2 (EZH2) is a key component of the polycomb repressive complex 2, which possesses histone methyltransferase activity and mediates gene silencing through posttranslational histone modifications[6]. EZH2 is frequently overexpressed in a wide variety of human malignancies such as breast cancer[7], prostate cancer[8], gastric cancer[9], colorectal cancer[10] and lung cancer It promotes cancer development and progression through chromatin modification by epigenetic activation of oncogenic signaling cascades and silencing of tumor suppressor genes, and has been implicated in cell proliferation, differentiation, invasion, and metastasis[11]. We conducted a meta-analysis of all available studies relating EZH2 with the clinical outcome in patients with lung cancer
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