Identification of CDC5L as bridge gene between chronic obstructive pulmonary disease and lung adenocarcinoma.

Identification of CDC5L as bridge gene between chronic obstructive pulmonary disease and lung adenocarcinoma.
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鉴定CDC5L作为慢性阻塞性肺疾病和肺腺癌之间的桥梁基因。

DOI:
10.2217/epi-2020-0112
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发表时间:
2020-06
期刊:
影响因子:
3.8
通讯作者:
Yu Ben-Tong
Yu Ben-Tong
中科院分区:
医学4区
文献类型:
--
作者:
Zhou Rui-Hao;Zhang Jing-Tao;Chen Chan;Xu Zi-Hao;Lv Xiao-Bin;Ye Ling;Yu Ben-Tong

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目的:本研究旨在探讨慢性阻塞性肺疾病(COPD)和肺腺癌(LUAD)的遗传和表观遗传相似性。材料和方法:我们主要利用加权相关网络分析、蛋白质-蛋白质相互作用网络分析和枢轴分析等方法对两种疾病的中枢模块、桥调节子、桥基因和中枢驱动基因进行了识别,并利用外部数据集进行了验证。结果:我们鉴定了8个桥梁调节因子,COPD模型中的19个关键分子和LUAD模型中的10个关键分子。此外,我们验证了CDC 5L可能是COPD的可靠生物标志物,并可能通过启动子甲基化调节LUAD的细胞增殖和转移。结论:本研究结果为今后在表观遗传水平上的研究奠定了理论基础。
Aim: This study aimed to explore the genetic and epigenetic similarities between chronic obstructive pulmonary disease (COPD) and lung adenocarcinoma (LUAD). Materials & methods: We mainly used Weighted correlation network analysis, protein-protein interaction network and pivot analysis to identify hub modules, bridge regulators, bridge genes and hub-driving genes in both diseases and carried out verifying using external datasets. Results: We identified eight bridge regulators, 19 key molecules in the COPD model and ten key molecules in the LUAD model. Moreover, we validated that CDC5L could be a reliable biomarker in COPD and may regulate cell proliferation and metastasis in LUAD via promoter methylation. Conclusion: Our results might form a theoretical foundation for future study at an epigenetic level.
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