The EZH overexpression group exhibited upregulated

The EZH2 overexpression group exhibited upregulated CEP55 expression but downregulated methylation, suggesting that changes in EZH2 expression in lung adenocarcinoma result in differences of CEP55 methylation and expression. Moreover, according to TCGA database and GSE27262 chip data, CEP55 expression is positively correlated with EZH2 expression, indicating that differential CEP55 expression in lung adenocarcinoma is related to EZH2 expression. As an epigenetic modifying factor, EZH2 promotes cancer by inhibiting the expression of tumour suppressor genes. For instance, EZH2 suppresses the expression of the antiangiogenic factor vasohibin 1 (VASH1) by elevating its methylation to promote tumour angiogenesis [29]. In addition, EZH2 affects cancer by activating oncogenes. EZH2 activates Ephrin-B2 expression by binding to the Ephrin-B2 promoter region to enhance tumour angiogenesis [16]. EZH2 expression increases the RAF1 gene copy number to activate the RAF1-ERK-β-catenin signalling pathway to promote the progression of breast cancer [8]. Consistent with our results, EZH2 overexpression affects lung adenocarcinoma by upregulating CEP55 expression. Moreover, according to the functional analysis, CEP55 was enriched in the entry of biological processes related to mitosis of mitotic nuclear division, mitotic metaphase plate congression, and mitotic cytokinesis. CEP55 is a type of mitotic phosphoprotein that plays a vital role in cell division. In the last stage of cell division, the physical separation of two daughter Medroxyprogesterone is achieved [43]. Therefore, CEP55 may affect the progression of cancer by altering the biological behaviour of cancer cells. To understand the potential of the differential expression of EZH2 and CEP55 acting as biomarkers for the prognosis of lung adenocarcinoma, survival curves for EZH2 and CEP55 expression were constructed. Changes in EZH2 expression could not accurately predict the prognosis of patients with lung adenocarcinoma. However, a previous study proved that a higher EZH2 expression level is associated with relapse-free and overall survival of patients with lung adenocarcinoma [4]. Cao et al. revealed that EZH2 is upregulated (compared with normal tissues) in non-small cell lung cancer (NSCLC) tissues and is an independent factor of a poor prognosis of these patients. However, interestingly, EZH2 expression itself in tumour tissues is not able to predict the prognosis of patients with NSCLC [6]. It remains to be determined whether EZH2 is a prognostic factor of lung adenocarcinoma in a large-scale analysis. Moreover, we also found that higher CEP55 expression represents a poorer prognosis of patients with lung adenocarcinoma, suggesting that CEP55 could serve as a prognostic factor for patients with lung adenocarcinoma. Several studies have revealed that CEP55 overexpression is considered a potential adverse prognostic factor for multiple cancers, including epithelial ovarian cancer [52], oesophageal squamous cancer [24], and pancreatic cancer [34]. Moreover, after radical resection in primary lung adenocarcinoma, CEP55 exhibited some prognostic significance [23]. We conclude that CEP55 is correlated with the prognosis of patients with lung adenocarcinoma and CEP55 expression and methylation are regulated by EZH2, providing a new target for clinical research and the treatment of lung adenocarcinoma.
Conclusion
Competing interests
Acknowledgments This study was supported by The PhD Start-up Fund of The First People’s Hospital of LianYunGang (BS1604). We would like to acknowledge the helpful comments on this paper received from our reviewers.
Introduction Gastric cancer is one of the most common human cancers and still remains the second most common cause of cancer mortality worldwide, despite decreasing incidence and mortality rates in developed countries over the past 20 years [1,2]. Although the majority of the patients at an early stage of gastric carcinoma can be cured by surgery, more than half of those at an advanced stage of this disease die of carcinoma recurrence, even after undergoing curative gastrectomy [3]. In spite of a great advancement on the research of gastric cancer, the molecular mechanisms underlying gastric cancer development and metastasis are still poorly understood. Therefore, a better understanding of the pathogenesis and identification of the molecular alterations is essential for the development of diagnostic markers that aid novel effective therapies for gastric cancer [4,5].