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Int J Clin Exp Pathol. 2014 Nov 26;7(12):8666-74. eCollection 2014.
2
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3
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Synergistic silencing by promoter methylation and reduced AP-2α transactivation of the proapoptotic HRK gene confers apoptosis resistance and enhanced tumor growth.促凋亡 HRK 基因启动子甲基化和 AP-2α 转录激活减少的协同沉默导致细胞凋亡抵抗和肿瘤生长增强。
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Mol Med Rep. 2014 Jul;10(1):467-72. doi: 10.3892/mmr.2014.2197. Epub 2014 Apr 29.

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本文引用的文献

1
AP-2α suppresses invasion in BeWo cells by repression of matrix metalloproteinase-2 and -9 and up-regulation of E-cadherin.AP-2α 通过抑制基质金属蛋白酶-2 和 -9 以及上调 E-钙黏蛋白来抑制 BeWo 细胞的侵袭。
Mol Cell Biochem. 2013 Sep;381(1-2):31-9. doi: 10.1007/s11010-013-1685-8. Epub 2013 May 10.
2
Transcription factor AP-2α regulates acute myeloid leukemia cell proliferation by influencing Hoxa gene expression.转录因子 AP-2α 通过影响 Hoxa 基因的表达来调节急性髓系白血病细胞的增殖。
Int J Biochem Cell Biol. 2013 Aug;45(8):1647-56. doi: 10.1016/j.biocel.2013.04.024. Epub 2013 May 6.
3
Synergistic silencing by promoter methylation and reduced AP-2α transactivation of the proapoptotic HRK gene confers apoptosis resistance and enhanced tumor growth.促凋亡 HRK 基因启动子甲基化和 AP-2α 转录激活减少的协同沉默导致细胞凋亡抵抗和肿瘤生长增强。
Am J Pathol. 2013 Jan;182(1):84-95. doi: 10.1016/j.ajpath.2012.09.018. Epub 2012 Nov 13.
4
Catalytic activity of Matrix metalloproteinase-19 is essential for tumor suppressor and anti-angiogenic activities in nasopharyngeal carcinoma.基质金属蛋白酶-19 的催化活性对于鼻咽癌中的肿瘤抑制和抗血管生成活性至关重要。
Int J Cancer. 2011 Oct 15;129(8):1826-37. doi: 10.1002/ijc.25855. Epub 2011 Apr 1.
5
MicroRNA145 targets BNIP3 and suppresses prostate cancer progression.miR-145 靶向 BNIP3 并抑制前列腺癌进展。
Cancer Res. 2010 Apr 1;70(7):2728-38. doi: 10.1158/0008-5472.CAN-09-3718. Epub 2010 Mar 23.
6
AP-2alpha Inhibits c-MYC Induced Oxidative Stress and Apoptosis in HaCaT Human Keratinocytes.AP-2alpha 抑制 c-MYC 诱导的 HaCaT 人角质形成细胞氧化应激和细胞凋亡。
J Oncol. 2009;2009:780874. doi: 10.1155/2009/780874. Epub 2009 Dec 24.
7
Molecular markers associated with lymph node metastasis in pancreatic ductal adenocarcinoma by genome-wide expression profiling.基于全基因组表达谱分析的胰腺导管腺癌淋巴结转移相关的分子标志物。
Cancer Sci. 2010 Jan;101(1):259-66. doi: 10.1111/j.1349-7006.2009.01359.x. Epub 2009 Sep 10.
8
Tumour growth and resistance to gemcitabine of pancreatic cancer cells are decreased by AP-2alpha overexpression.AP-2α过表达可降低胰腺癌细胞的肿瘤生长及对吉西他滨的耐药性。
Br J Cancer. 2009 Aug 18;101(4):637-44. doi: 10.1038/sj.bjc.6605190.
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BCL-xL is a target gene regulated by hypoxia-inducible factor-1{alpha}.BCL-xL是一种受缺氧诱导因子-1α调控的靶基因。
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10
Shift in AP-2alpha localization characterizes astrocytoma progression.AP-2α定位的改变是星形细胞瘤进展的特征。
Cancer Biol Ther. 2007 Mar;6(3):413-8. doi: 10.4161/cbt.6.3.3756. Epub 2007 Mar 28.

AP-2α转录因子的异位表达抑制胶质瘤进展。

Ectopic expression of AP-2α transcription factor suppresses glioma progression.

作者信息

Su Wenjing, Xia Juan, Chen Xueqin, Xu Miao, Nie Ling, Chen Ni, Gong Jing, Li Xinglan, Zhou Qiao

机构信息

Laboratory of Pathology, State Key Laboratory of Biotherapy and Department of Pathology, West China Hospital, West China Medical School, Sichuan University Chengdu 610041, China.

Laboratory of Pathology, State Key Laboratory of Biotherapy and Department of Pathology, West China Hospital, West China Medical School, Sichuan University Chengdu 610041, China ; Suining Central Hospital Suining 629000, China.

出版信息

Int J Clin Exp Pathol. 2014 Nov 26;7(12):8666-74. eCollection 2014.

PMID:25674231
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4314016/
Abstract

The transcriptional factor AP-2α is a tumor suppressor gene and is downregulated in various neoplasms including glioma. Although the level of AP-2α is negatively associated with the grade of human glioma, the specific functions of AP-2α in glioma are still unknown. In this study, we experimentally showed that artificial overexpression of AP-2α in glioma T98G and U251 cells significantly downregulated the mRNA levels of Bcl-xl, Bcl-2, c-IAP2 and survivin, together with upregulation of the Hrk mRNA levels. Reintroduction of AP-2α also induced downregulation of the protein levels of survivin and VEGF in glioma cells. In biological assays with T98G and U251 cells, AP-2α reduced tumor cell growth, increased cell death, attenuated cell migration and endothelial tube formation. The AP-2α transcription factor may play an important role in suppressing glioma progression.

摘要

转录因子AP - 2α是一种肿瘤抑制基因,在包括胶质瘤在内的多种肿瘤中表达下调。尽管AP - 2α的水平与人类胶质瘤的分级呈负相关,但其在胶质瘤中的具体功能仍不清楚。在本研究中,我们通过实验表明,在胶质瘤T98G和U251细胞中人工过表达AP - 2α可显著下调Bcl - xl、Bcl - 2、c - IAP2和survivin的mRNA水平,同时上调Hrk的mRNA水平。重新引入AP - 2α也可诱导胶质瘤细胞中survivin和VEGF蛋白水平的下调。在对T98G和U251细胞进行的生物学实验中,AP - 2α可减少肿瘤细胞生长、增加细胞死亡、减弱细胞迁移和内皮管形成。AP - 2α转录因子可能在抑制胶质瘤进展中发挥重要作用。