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SATB1对乳腺癌中长链非编码RNA UCA1的表观遗传调控

Epigenetic regulation of long noncoding RNA UCA1 by SATB1 in breast cancer.

作者信息

Lee Jong-Joo, Kim Mikyoung, Kim Hyoung-Pyo

机构信息

Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College of Medicine; Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul 03722, Korea.

Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College of Medicine, Seoul 03722, Korea.

出版信息

BMB Rep. 2016 Oct;49(10):578-583. doi: 10.5483/bmbrep.2016.49.10.156.

DOI:10.5483/bmbrep.2016.49.10.156
PMID:27697109
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5227301/
Abstract

Special AT-rich sequence binding protein 1 (SATB1) is a nuclear matrix-associated DNA-binding protein that functions as a chromatin organizer. SATB1 is highly expressed in aggressive breast cancer cells and promotes growth and metastasis by reprograming gene expression. Through genomewide cross-examination of gene expression and histone methylation, we identified SATB1 target genes for which expression is associated with altered epigenetic marks. Among the identified genes, long noncoding RNA urothelial carcinoma-associated 1 (UCA1) was upregulated by SATB1 depletion. Upregulation of UCA1 coincided with increased H3K4 trimethylation (H3K4me3) levels and decreased H3K27 trimethylation (H3K27me3) levels. Our study showed that SATB1 binds to the upstream region of UCA1 in vivo, and that its promoter activity increases with SATB1 depletion. Furthermore, simultaneous depletion of SATB1 and UCA1 potentiated suppression of tumor growth and cell survival. Thus, SATB1 repressed the expression of oncogenic UCA1, suppressing growth and survival of breast cancer cells. [BMB Reports 2016; 49(10): 578-583].

摘要

富含AT序列结合蛋白1（SATB1）是一种与核基质相关的DNA结合蛋白，作为染色质组织者发挥作用。SATB1在侵袭性乳腺癌细胞中高度表达，并通过重编程基因表达促进生长和转移。通过对基因表达和组蛋白甲基化进行全基因组交叉检查，我们鉴定出了SATB1的靶基因，其表达与表观遗传标记的改变相关。在鉴定出的基因中，长链非编码RNA尿路上皮癌相关1（UCA1）在SATB1缺失时上调。UCA1的上调与H3K4三甲基化（H3K4me3）水平升高和H3K27三甲基化（H3K27me3）水平降低同时出现。我们的研究表明，SATB1在体内与UCA1的上游区域结合，并且其启动子活性随着SATB1的缺失而增加。此外，同时缺失SATB1和UCA1可增强对肿瘤生长和细胞存活的抑制作用。因此，SATB1抑制致癌性UCA1的表达，从而抑制乳腺癌细胞的生长和存活。[《BMB报告》2016年；49(10):578 - 583]

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/fded10777fc3/BMB-49-578-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/6259c6e97ff5/BMB-49-578-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/426aad93b504/BMB-49-578-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/4eca7daf29d7/BMB-49-578-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/fded10777fc3/BMB-49-578-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/6259c6e97ff5/BMB-49-578-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/426aad93b504/BMB-49-578-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/4eca7daf29d7/BMB-49-578-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd1c/5227301/fded10777fc3/BMB-49-578-g004.jpg

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