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Protein kinase A RIalpha antisense inhibition of PC3M prostate cancer cell growth: Bcl-2 hyperphosphorylation, Bax up-regulation, and Bad-hypophosphorylation.蛋白激酶A RIα反义抑制PC3M前列腺癌细胞生长：Bcl-2过度磷酸化、Bax上调和Bad去磷酸化。
Clin Cancer Res. 2002 Feb;8(2):607-14.
2
Application of cDNA microarrays to examine gene expression differences in schizophrenia.应用cDNA微阵列检测精神分裂症中的基因表达差异。
Brain Res Bull. 2001 Jul 15;55(5):641-50. doi: 10.1016/s0361-9230(01)00522-6.
3
Developmental regulation and overexpression of the transcription factor AP-2, a potential regulator of the timing of Schwann cell generation.转录因子AP-2的发育调控与过表达，施万细胞生成时间的潜在调节因子
Eur J Neurosci. 2001 Jul;14(2):363-72. doi: 10.1046/j.0953-816x.2001.01650.x.
4
Antisense DNAs as multisite genomic modulators identified by DNA microarray.通过DNA微阵列鉴定的作为多位点基因组调节剂的反义DNA
Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9819-23. doi: 10.1073/pnas.171314398. Epub 2001 Jul 31.
5
Apoptosis, growth arrest and suppression of invasiveness by CRE-decoy oligonucleotide in ovarian cancer cells: protein kinase A downregulation and cytoplasmic export of CRE-binding proteins.
Mol Cell Biochem. 2001 Feb;218(1-2):55-63. doi: 10.1023/a:1007205205131.
6
Reduction in cyclin D1/Cdk4/retinoblastoma protein signaling by CRE-decoy oligonucleotide.通过CRE诱饵寡核苷酸降低细胞周期蛋白D1/细胞周期蛋白依赖性激酶4/视网膜母细胞瘤蛋白信号传导
Biochem Biophys Res Commun. 2001 Mar;281(5):1213-9. doi: 10.1006/bbrc.2001.4521.
7
How do you see CG?你如何看待CG？
Cell. 2000 Dec 22;103(7):993-6. doi: 10.1016/s0092-8674(00)00201-4.
8
Regulatory roles of AP-2 transcription factors in vertebrate development, apoptosis and cell-cycle control.AP-2转录因子在脊椎动物发育、细胞凋亡和细胞周期调控中的调节作用。
Gene. 2000 Dec 30;260(1-2):1-12. doi: 10.1016/s0378-1119(00)00454-6.
9
CRE-decoy oligonucleotide-inhibition of gene expression and tumor growth.CRE-诱饵寡核苷酸对基因表达和肿瘤生长的抑制作用
Mol Cell Biochem. 2000 Sep;212(1-2):29-34.
10
YY1 as a regulator of replication-dependent hamster histone H3.2 promoter and an interactive partner of AP-2.YY1作为复制依赖性仓鼠组蛋白H3.2启动子的调节因子以及AP-2的相互作用伴侣。
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环磷酸腺苷反应元件增强子诱饵的基因组规模视图：一种基于肿瘤靶点的基因工具。

A genomic-scale view of the cAMP response element-enhancer decoy: a tumor target-based genetic tool.

作者信息

Cho Yee Sook, Kim Meyoung-Kon, Cheadle Chris, Neary Catherine, Park Yun Gyu, Becker Kevin G, Cho-Chung Yoon S

机构信息

Cellular Biochemistry Section, Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15626-31. doi: 10.1073/pnas.242617799. Epub 2002 Nov 18.

DOI:10.1073/pnas.242617799
PMID:12438686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC137767/
Abstract

Enhancer DNA decoy oligodeoxynucleotides (ODNs) inhibit transcription by competing for transcription factors. A decoy ODN composed of the cAMP response element (CRE) inhibits CRE-directed gene transcription and tumor growth without affecting normal cell growth. Here, we use DNA microarrays to analyze the global effects of the CRE-decoy ODN in cancer cell lines and in tumors grown in nude mice. The CRE-decoy up-regulates the AP-2beta transcription factor gene in tumors but not in the livers of host animals. The up-regulated expression of AP-2beta is clustered with the up-regulation of other genes involved in development and cell differentiation. Concomitantly, another cluster of genes involved in cell proliferation and transformation is down-regulated. The observed alterations indicate that CRE-directed transcription favors tumor growth. The CRE-decoy ODN, therefore, may serve as a target-based genetic tool to treat cancer and other diseases in which CRE-directed transcription is abnormally used.

摘要

增强子DNA诱饵寡脱氧核苷酸（ODN）通过竞争转录因子来抑制转录。一种由环磷酸腺苷反应元件（CRE）组成的诱饵ODN可抑制CRE指导的基因转录和肿瘤生长，而不影响正常细胞生长。在此，我们使用DNA微阵列分析CRE诱饵ODN对癌细胞系和裸鼠体内生长肿瘤的整体影响。CRE诱饵在肿瘤中上调AP-2β转录因子基因，但在宿主动物的肝脏中则不然。AP-2β的上调表达与其他参与发育和细胞分化的基因上调聚集在一起。同时，另一组参与细胞增殖和转化的基因被下调。观察到的变化表明，CRE指导的转录有利于肿瘤生长。因此，CRE诱饵ODN可作为一种基于靶点的基因工具，用于治疗癌症和其他异常使用CRE指导转录的疾病。