GSE1 通过下调 KLF6 的表达促进肺腺癌细胞的增殖和迁移。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Ziyu Meng, Yingqian Yang, Shupei Li, Liguo Huang, Zhoujuan Yao, Yixuan Chen, Junkun Wang, Yiru Shen, Pingping Liang, Hui Zhang, Wenbin Wang, Fengsong Wang
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引用次数: 0

摘要

肺癌是全球发病率最高的人类癌症之一,致死率很高。在这项研究中,我们证实了 GSE1(遗传抑制因子 1)在肺腺癌中的表达异常上调,并且 GSE1 的缺失抑制了 A549 和 H1299 细胞的增殖和迁移。免疫沉淀试验表明,GSE1 与细胞中的组蛋白去乙酰化酶 1(HDAC1)及其他 BRAF-HDAC 复合物(BHC)成分相互作用。GSE1 敲除的 A549 细胞转录组显示,207 个基因上调,159 个基因下调,p 值为 0.05。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
GSE1 promotes the proliferation and migration of lung adenocarcinoma cells by downregulating KLF6 expression

Lung cancer is one of the most prevalent human cancers with a high lethality rate worldwide. In this study, we demonstrated that GSE1 (genetic suppressor element 1) expression is aberrantly upregulated in lung adenocarcinoma and that GSE1 depletion inhibits the proliferation and migration of both A549 and H1299 cells. Immunoprecipitation assays demonstrated that GSE1 interacts with histone deacetylase 1 (HDAC1) and other BRAF–HDAC complex (BHC) components in cells. The transcriptome of GSE1-knockdown A549 cells indicated that 207 genes were upregulated and 159 were downregulated based on a p-value < .05 and fold change ≥ 1.5. Bioinformatics analysis suggested that 140 differentially expressed genes harbor binding sites for HDAC1, including the tumor suppressor gene KLF6 (Kruppel-like factor 6). Indeed, quantitative reverse-transcription polymerase chain reaction and western blot analysis revealed that GSE1 could inhibit the transcription of KLF6 in lung cancer cells. In conclusion, GSE1 cooperates with HDAC1 to promote the proliferation and metastasis of non-small cell lung cancer cells through the downregulation of KLF6 expression.

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来源期刊
Cell Biology International
Cell Biology International 生物-细胞生物学
CiteScore
7.60
自引率
0.00%
发文量
208
审稿时长
1 months
期刊介绍: Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.
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