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GEO help: Mouse over screen elements for information. |
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Status |
Public on Jun 01, 2017 |
Title |
FOXN3 and SIN3A ChIP-Seq; FOXN3 and IgG iRIP-Seq |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing Non-coding RNA profiling by high throughput sequencing
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Summary |
The forkhead box (FOX) family of proteins is composed of more than 50 members that are phylogenetically classified into 19 subclasses (A to S). These transcription factors all share a homology in their DNA-binding domain, the forkhead domain, also known as winged helix due to its butterfly-like structural appearance.FOX proteins have been implicated in a broad spectrum of cellular processes including cell proliferation, differentiation, DNA repair, metabolism, and aging. However, the biological function of the mammalian forkhead transcription factors of the N class including FOXN3 remains to be investigated. The SIN3A complex is a large protein assembly consisting of over a dozen of proteins including SIN3A, HDAC1/2, RBBP4/7 and etc. This complex is recruited by multiple transcription repressors and impacts on multifaceted biological functions ranging from development, differentiation, and senescence to oncogenic transformation. Long noncoding RNAs (lncRNAs) are a class of noncoding RNAs that are over 200 nucleotides in length. In the past years, these molecules have emerged as important components of the epigenetic regulatory network to influence transcription as well as other nuclear activities, and their dysregulation underlies several pathologic states including cancer. One of the lncRNAs, NEAT1 (nuclear paraspeckle assembly transcript 1), is a highly abundant lncRNA initially described as a structural component of nuclear paraspeckles. Subsequent studies suggest that NEAT1 also influences transcription through either an indirect mechanism or a direct way. In this study, we investigated the function and the underlying mechanism of FOXN3 in breast cancer cells. We showed that FOXN3 is physically associated with the SIN3A complex and identified that NEAT1, which is induced by estrogen in breast cancer cells, is required for this interaction. We analyzed the genomic targets of the FOXN3/SIN3A/NEAT1 complex and demonstrated that estrogen receptor (ER) itself is regulated, through negative feedback, by the FOXN3/SIN3A/NEAT1 complex. We investigated the role of the FOXN3/SIN3A/NEAT1 complex in breast cancer metastasis and explored the clinicopathological significance of the ER-NEAT1-FOXN3/NEAT1/SIN3A-GATA3 axis in breast cancer.
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Overall design |
The Genome-wide binding profiles of FOXN3 and SIN3A in MCF-7 cells were determined by Chromatin Immunoprecipitation followed by high-throughput sequencing (ChIP-Seq). Besides, the potential lncRNAs that is required for the interaction of the SIN3A complex with FOXN3 were identified by an Improved RNA ImmunoPrecipitation-coupled high-throughput sequencing (iRIP-seq) method with antibodies against FOXN3.
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Contributor(s) |
Li W, Zhang Z |
Citation(s) |
28805661 |
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Submission date |
Jan 18, 2017 |
Last update date |
Jul 19, 2019 |
Contact name |
Wanjin Li |
E-mail(s) |
[email protected]
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Phone |
13622157177
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Organization name |
Peking University Health Science Center
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Street address |
No. 38, Xueyuan road.
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City |
Beijing |
ZIP/Postal code |
100191 |
Country |
China |
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Platforms (1) |
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Samples (7)
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This SubSeries is part of SuperSeries: |
GSE93781 |
FOXN3 Enlists NEAT1-containing SIN3A Complex to Regulate Mammary Epithelium Differentiation and Promote Breast Cancer Metastasis |
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Relations |
BioProject |
PRJNA362507 |
SRA |
SRP100560 |
Supplementary file |
Size |
Download |
File type/resource |
GSE93780_CIMS_Rep1.bed.gz |
42.4 Kb |
(ftp)(http) |
BED |
GSE93780_CIMS_Rep2.bed.gz |
31.9 Kb |
(ftp)(http) |
BED |
GSE93780_Piranha_Rep1.bed.gz |
19.2 Kb |
(ftp)(http) |
BED |
GSE93780_Piranha_Rep2.bed.gz |
17.7 Kb |
(ftp)(http) |
BED |
GSE93780_RAW.tar |
501.1 Mb |
(http)(custom) |
TAR (of BW) |
SRA Run Selector |
Raw data are available in SRA |
Processed data provided as supplementary file |
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