IR@PKUHSC  > 北京大学临床肿瘤学院  > 病理科
学科主题临床医学
Regulatory mechanisms for abnormal expression of the human breast cancer specific gene 1 in breast cancer cells
Lu Aiping; Li Qing; Liu Jingwen
关键词breast cancer-specific gene 1 promoter transcriptional activity
刊名SCIENCE IN CHINA SERIES C-LIFE SCIENCES
2006-08-01
DOI10.1007/s11427-006-2006-1
49期:4页:403-408
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biology
研究领域[WOS]Life Sciences & Biomedicine - Other Topics
关键词[WOS]SYNUCLEIN-GAMMA ; ABERRANT EXPRESSION ; CPG ISLAND ; IDENTIFICATION ; TRANSCRIPTION ; CARCINOMA ; DISEASE
英文摘要

Breast cancer-specific gene 1 (BCSG1), also referred as synuclein gamma, was originally isolated from a human breast cancer cDNA library and the protein is mainly localized to presynaptic terminals in the nervous system. BCSG1 is not expressed in normal or benign breast lesions, but expressed at an extremely high level in the vast majority of the advanced staged breast carcinomas and ovarian carcinomas. Overexpression of BCSG1 in cancer cells led to significant increase in cell proliferation, motility and invasiveness, and metastasis. To elucidate the molecular mechanism and regulation for abnormal transcription of BCSG1, a variety of BCSG1 promoter luciferase reporters were constructed including 3 ′ end deleted sequences, Sp1 deleted, and activator protein-1 (AP1) domains mutated. Transient transfection assay was used to detect the transcriptional activation of BCSG1 promoters. Results showed that the Sp1 sequence in 5 ′-flanking region was involved in the basal transcriptional activities of BCSG1 without cell-type specificity. In comparison to pGL3-1249, the reporter activities of pGL3-1553 in BCSG1-negative MCF-7 cells and pGL3-1759 in HepG2 cells were notably decreased. Mutations at AP1 sites in BCSG1 intron 1 significantly reduced the promoter activity in all cell lines. Transcription factors, c-jun, c-fos and cyclin AMP-responsive element binding (CREB) protein, could markedly enhance the promoter activities. Thus, our results suggest that the abnormal expression of BCSG1 in breast cancer cells is likely regulated by multiple mechanisms. The 5 ′ flanking region of BCSG1 provides the basal transcriptional activity without cell type specificity. A critical promoter element involved in abnormal expression of BCSG1 presents in the first exon. The cell type specificity of BCSG1 transcription is probably affected through intronic cis-regulatory sequences. AP1 domains in the first intron play an important role in control of BCSG1 transcription.

语种英语
WOS记录号WOS:000240411800013
Citation statistics
Cited Times:2[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/60206
Collection北京大学临床肿瘤学院_病理科
作者单位1.VA Palo Alto Hlth Care Syst, Palo Alto, CA 94304 USA
2.Peking Univ, Sch Oncol, Beijing Canc Hosp, Dept Pathol, Beijing 100036, Peoples R China
Recommended Citation
GB/T 7714
Lu Aiping,Li Qing,Liu Jingwen. Regulatory mechanisms for abnormal expression of the human breast cancer specific gene 1 in breast cancer cells[J]. SCIENCE IN CHINA SERIES C-LIFE SCIENCES,2006,49(4):403-408.
APA Lu Aiping,Li Qing,&Liu Jingwen.(2006).Regulatory mechanisms for abnormal expression of the human breast cancer specific gene 1 in breast cancer cells.SCIENCE IN CHINA SERIES C-LIFE SCIENCES,49(4),403-408.
MLA Lu Aiping,et al."Regulatory mechanisms for abnormal expression of the human breast cancer specific gene 1 in breast cancer cells".SCIENCE IN CHINA SERIES C-LIFE SCIENCES 49.4(2006):403-408.
Files in This Item:
There are no files associated with this item.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
谷歌学术
谷歌学术Similar articles in
[Lu Aiping]'s Articles
[Li Qing]'s Articles
[Liu Jingwen]'s Articles
百度学术
百度学术Similar articles in
[Lu Aiping]'s Articles
[Li Qing]'s Articles
[Liu Jingwen]'s Articles
必应学术
必应学术Similar articles in
[Lu Aiping]'s Articles
[Li Qing]'s Articles
[Liu Jingwen]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.