NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE85579 Query DataSets for GSE85579
Status Public on Jun 10, 2017
Title Genomic Regulation of Invasion by STAT3 in Triple Negative Breast Cancer
Organism Homo sapiens
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Expression profiling by high throughput sequencing
Summary Breast cancer is a heterogeneous disease comprised of four molecular subtypes defined by whether the tumor-originating cells are luminal or basal epithelial cells. Breast cancers arising from the luminal mammary duct often express estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth receptor 2 (HER2). Tumors expressing ER and/or PR are treated with anti-hormonal therapies, while tumors overexpressing HER2 are targeted with monoclonal antibodies. Immunohistochemical detection of ER, PR, and HER2 receptors/proteins is a critical step in breast cancer diagnosis and guided treatment. Breast tumors that do not express these proteins are known as “triple negative breast cancer” (TNBC) and are typically basal-like. TNBCs are the most aggressive subtype, with the highest mortality rates and no targeted therapy, so there is a pressing need to identify important TNBC tumor regulators. The signal transducer and activator of transcription 3 (STAT3) transcription factor has been previously implicated as a constitutively active oncogene in TNBC. However, its direct regulatory gene targets and tumorigenic properties have not been well characterized. By integrating RNA-seq and ChIP-seq data from 2 TNBC tumors and 4 cell lines, we discovered novel gene signatures directly regulated by STAT3 that were enriched for processes involving inflammation, immunity, and invasion in TNBC. Functional analysis revealed that STAT3 has a key role regulating invasion and metastasis, a characteristic often associated with TNBC. Our findings suggest therapies targeting STAT3 may be important for preventing TNBC metastasis.
 
Overall design ChIP-seq and RNA-seq experimentation were performed in TNBC cell lines: HCC70, MDA-MB-231, MDA-MB-468, MDA-MB-157, HCC1143. ChIP-seq was performed after 1hr vehicle control indcution (ethanol). RNA-seq was performed after 96hr knockdown of STAT3 or non-targeting siRNA. Tissue ChIP-seq was performed in two TNBC tumor samples: A139 and A137.
 
Contributor(s) Myers RM
Citation(s) 28030809
Submission date Aug 13, 2016
Last update date Mar 20, 2019
Contact name Joy Agee
E-mail jagee@hudsonalpha.org
Phone 2059945492
Organization name HudsonAlpha Institute for Biotechnology
Street address 601 Genome Way
City Huntsville
State/province AL
ZIP/Postal code 35806
Country USA
 
Platforms (1)
GPL11154 Illumina HiSeq 2000 (Homo sapiens)
Samples (54)
GSM2278000 MDAMB157_STAT3_Rep1
GSM2278001 MDAMB157_STAT3_Rep2
GSM2278002 MDAMB231_STAT3_Rep1
Relations
BioProject PRJNA338851
SRA SRP081918

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE85579_HCC1143_STAT3_Lib_list.txt.SharedGeneCounts.txt.gz 840.2 Kb (ftp)(http) TXT
GSE85579_LibList_HCC70_STAT3_siRNA_96hr.txt.SharedGeneCounts.txt.gz 872.8 Kb (ftp)(http) TXT
GSE85579_LibList_MDA231_STAT3_siRNA_96hr.txt.SharedGeneCounts.txt.gz 878.6 Kb (ftp)(http) TXT
GSE85579_MDA468_MDA157_STAT3_Lib_List.txt.SharedGeneCounts.txt.gz 1.2 Mb (ftp)(http) TXT
GSE85579_RAW.tar 402.0 Mb (http)(custom) TAR (of BEDGRAPH)
Raw data are available in SRA
Processed data provided as supplementary file
Processed data is available on Series record

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap