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CtBP1基因沉默抑制人胶质瘤细胞的迁移。

Silencing of CtBP1 suppresses the migration in human glioma cells.

作者信息

Zhao Chengjin, Shen Yifen, Tao Xuelei, Xu Jian, Lu Junjie, Liu Chao, Xu Zhiwei, Tang Qing, Tao Tao, Zhang Xiubing

机构信息

Department of Neurosurgery, Nantong Second People Affiliated Hospital of Nantong University, 43 Xinglong Road, Nantong, 226001, Jiangsu Province, People's Republic of China.

Department of Immunology, Medical School of Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu Province, People's Republic of China.

出版信息

J Mol Histol. 2016 Jun;47(3):297-304. doi: 10.1007/s10735-016-9678-z. Epub 2016 May 9.

DOI:10.1007/s10735-016-9678-z
PMID:27160109
Abstract

Carboxyl-terminal binding protein 1 (CtBP1), up-regulated in various types of human cancers, has been functionally associated with proliferation, anti-apoptosis, and EMT in vitro studies. However, the functional significance of CtBP1 in the pathophysiology of glioma remains unknown. In the present study, we showed the expression of CtBP1 was markedly higher in glioma tissues compared with normal brain tissues by Western blot analysis. Immunohistochemical analysis revealed that CtBP1 mainly localized in the nucleus of glioma cells. Statistical analysis suggested the upregulation of CtBP1 was considerably correlated with the WHO grade (P < 0.05) and those patients with high CtBP1 levels exhibited shorter survival time (P < 0.01). Silencing CtBP1 by short hairpin RNAi caused an inhibition of cell migration. Moreover, knockdown of CtBP1 increases E-cadherin expression and decreases vimentin expression. These data uncovered that CtBP1 protein is a valuable marker of glioma pathogenic process and that CtBP1 can serve as a novel prognostic marker for glioma therapy.

摘要

羧基末端结合蛋白1(CtBP1)在多种人类癌症中上调,在体外研究中其功能与增殖、抗凋亡和上皮-间质转化相关。然而,CtBP1在胶质瘤病理生理学中的功能意义仍不清楚。在本研究中,我们通过蛋白质印迹分析表明,与正常脑组织相比,胶质瘤组织中CtBP1的表达明显更高。免疫组织化学分析显示,CtBP1主要定位于胶质瘤细胞的细胞核中。统计分析表明,CtBP1的上调与世界卫生组织(WHO)分级显著相关(P<0.05),且CtBP1水平高的患者生存时间较短(P<0.01)。通过短发夹RNA干扰沉默CtBP1会导致细胞迁移受到抑制。此外,敲低CtBP1会增加E-钙黏蛋白的表达并降低波形蛋白的表达。这些数据揭示,CtBP1蛋白是胶质瘤致病过程的一个有价值的标志物,并且CtBP1可作为胶质瘤治疗的一种新的预后标志物。

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本文引用的文献

1
Eph receptors as therapeutic targets in glioblastoma.作为胶质母细胞瘤治疗靶点的Eph受体
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2
Stem cell characteristics in glioblastoma are maintained by the ecto-nucleotidase E-NPP1.胶质母细胞瘤中的干细胞特征由胞外核苷酸酶E-NPP1维持。
Cell Death Differ. 2014 Jun;21(6):929-40. doi: 10.1038/cdd.2014.12. Epub 2014 Feb 14.
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Systematic review of protein biomarkers of invasive behavior in glioblastoma.胶质母细胞瘤侵袭行为的蛋白质生物标志物的系统评价
急性暴露于甲基汞对蠵龟红细胞的转录分析
Toxics. 2021 Mar 29;9(4):70. doi: 10.3390/toxics9040070.
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C-terminal of E1A binding protein 1 enhances the migration of gastric epithelial cells and has a clinicopathologic significance in human gastric carcinoma.E1A结合蛋白1的C末端增强胃上皮细胞的迁移并在人胃癌中具有临床病理意义。
Onco Targets Ther. 2019 Jul 2;12:5189-5200. doi: 10.2147/OTT.S203479. eCollection 2019.
5
C-terminal of E1A binding protein 2 promotes the malignancy of osteosarcoma cells via JAK1/Stat3 signaling.E1A结合蛋白2的C末端通过JAK1/Stat3信号通路促进骨肉瘤细胞的恶性增殖。
J Cell Commun Signal. 2020 Mar;14(1):67-76. doi: 10.1007/s12079-019-00523-9. Epub 2019 Jun 19.
6
CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma.CtBP1 与 SOX2 相互作用,促进肺腺癌的生长、迁移和侵袭。
Oncol Rep. 2019 Jul;42(1):67-78. doi: 10.3892/or.2019.7142. Epub 2019 May 2.
7
Dysregulation of Macropinocytosis Processes in Glioblastomas May Be Exploited to Increase Intracellular Anti-Cancer Drug Levels: The Example of Temozolomide.胶质母细胞瘤中巨胞饮作用过程的失调可能被利用来提高细胞内抗癌药物水平:以替莫唑胺为例。
Cancers (Basel). 2019 Mar 22;11(3):411. doi: 10.3390/cancers11030411.
8
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Mol Neurobiol. 2014 Jun;49(3):1212-44. doi: 10.1007/s12035-013-8593-5. Epub 2013 Nov 24.
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J Mol Histol. 2014 Apr;45(2):141-51. doi: 10.1007/s10735-013-9540-5. Epub 2013 Sep 13.
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9
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10
Transcriptional down-regulation of Brca1 and E-cadherin by CtBP1 in breast cancer.CtBP1 对乳腺癌中 Brca1 和 E-cadherin 的转录下调作用。
Mol Carcinog. 2012 Jun;51(6):500-7. doi: 10.1002/mc.20813. Epub 2011 Jun 16.