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叉头框A1的敲低通过调节磷酸酶和张力蛋白同源物/蛋白激酶B通路抑制人结肠癌细胞的肿瘤发生和进展。

Knockdown of Forkhead box A1 suppresses the tumorigenesis and progression of human colon cancer cells through regulating the phosphatase and tensin homolog/Akt pathway.

作者信息

Pan Jie, Xu Zongbin, Xu Meifang, Lin Xiaoyan, Lin Bingqiang, Lin Mengxin

机构信息

Department of General Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, P.R. China.

Department of Pathology, Fujian Medical University Union Hospital, Fuzhou, Fujian, P.R. China.

出版信息

J Int Med Res. 2020 Dec;48(12):300060520971453. doi: 10.1177/0300060520971453.

Abstract

BACKGROUND

This study aimed to evaluate the role and the underlying mechanisms of Forkhead box A1 (encoded by ) in colon cancer.

METHODS

We analyzed mRNA and protein expression in colon cancer tissues and cell lines. We also silenced expression in HCT116 and SW480 cells to evaluate the effects on cell proliferation, cell cycle, migration, and invasion by using MTT, colony formation, flow cytometry, and the Transwell assay, respectively.

RESULTS

FOXA1 immunostaining was higher in colon cancer tissues than adjacent healthy tissues. mRNA and protein expression was significantly increased in human colon cancer cells compared with a normal colonic cell line. expression was also significantly higher in colorectal cancer tissues from TCGA data sets and was associated with worse prognosis in the R2 database. expression was negatively correlated with the extent of its methylation, and its knockdown reduced proliferation, migration, and invasion, and induced G2/M phase arrest in HCT116 and SW480 cells by suppressing the phosphatase and tensin homolog/Akt signaling pathway and inhibiting epithelial-mesenchymal transition.

CONCLUSION

may act as an oncogene in colon cancer tumorigenesis and development.

摘要

背景

本研究旨在评估叉头框A1(由[具体基因名称]编码)在结肠癌中的作用及潜在机制。

方法

我们分析了结肠癌组织和细胞系中[具体基因名称]的mRNA和蛋白表达。我们还在HCT116和SW480细胞中沉默[具体基因名称]的表达,分别使用MTT、集落形成、流式细胞术和Transwell实验来评估对细胞增殖、细胞周期、迁移和侵袭的影响。

结果

结肠癌组织中FOXA1免疫染色高于相邻健康组织。与正常结肠细胞系相比,人结肠癌细胞中[具体基因名称]的mRNA和蛋白表达显著增加。来自TCGA数据集的结直肠癌组织中[具体基因名称]的表达也显著更高,并且在R2数据库中与较差的预后相关。[具体基因名称]的表达与其甲基化程度呈负相关,其敲低通过抑制磷酸酶和张力蛋白同源物/Akt信号通路并抑制上皮-间质转化,降低了HCT116和SW480细胞的增殖、迁移和侵袭,并诱导G2/M期阻滞。

结论

[具体基因名称]在结肠癌的发生和发展中可能作为一种癌基因发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1193/7731712/c556b14ec544/10.1177_0300060520971453-fig1.jpg

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