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SRP058490
Homo sapiens
8 Downloadable Samples
IonTorrentProton
Description
The canonical Wnt pathway plays a central role in stem cell maintenance, differentiation and proliferation in the intestinal epithelium. Constitutive, aberrant activity of the TCF4/ß-catenin transcriptional complex is the primary transforming factor in colorectal cancer. Despite significant recent inroads, the full complement of Wnt target genes and the mechanisms of regulation remain incompletely understood. Here we identify a nuclear long non-coding RNA, termed WiNTRLINC1, as a direct target of TCF4/ß-catenin in colorectal cancer cells. WiNTRLINC1 positively regulates the expression of its close neighbor ASCL2, a transcription factor that controls intestinal stem cell fate. WiNTRLINC1 interacts with TCF4/ß-catenin to mediate the juxtaposition/physical contact of its own promoter with the regulatory regions of ASCL2. ASCL2, in turn, regulates WiNTRLINC1 expression. This feedforward regulatory loop controls stem cell-related gene expression and is highly amplified in colorectal cancer. Overall design: Derivatives of Ls174T colon cancer cells, overexpressing the Tet repressor were used for the construction of inducible overexpressing a shRNA against the WiNTRLINC1 long non coding RNA upon treatment with doxyxycline. siRNAs against WiNTRLINC1 were designed with the siDesign center tool from Dharmacon and their sequences were used for the construction of the shRNA stem loop structure as described in EMBO Rep. 2003 Jun;4(6):609-15. The modified pTER vector was used as a backbone for constructing the shRNA cassette as described in EMBO Rep. 2003 Jun;4(6):609-15. Positive cell clones were screened with RT-PCR in order to validate the efficiency of the knockdown of WiNTRLINC1. The Ls174T derivative cell line inducibly overexpressing a shRNA against ASCL2 has been described previously in Cell. 2009 Mar 6;136(5):903-12. RNA deep sequencing was performed in the WiNTRLINC1 KD and ASCL2 KD cells compared to controls cells in order to detect changes in gene expression due to the loss of either WiNTRLINC1 or ASCL2.
Publication Title
A Positive Regulatory Loop between a Wnt-Regulated Non-coding RNA and ASCL2 Controls Intestinal Stem Cell Fate.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 5 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We compared different mouse cancer cell lines to identify their unique cell signatures.
Publication Title
Mutant KRAS promotes malignant pleural effusion formation.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 5 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We compared different mouse cancer cell lines to identify their unique cell signatures.
Publication Title
Mutant KRAS promotes malignant pleural effusion formation.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 1 Downloadable Sample
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
We isolated mouse epithelial trachea cells from FVB mice in order to identify their transcriptomic signature.
Publication Title
Mutant KRAS promotes malignant pleural effusion formation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Mast cells mediate malignant pleural effusion formation.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Nave mast cells were cultured from murine bone marrow using incubation with IL-3 alone (samples 1-4) or IL-3 and KITL (samples 5-8).
Publication Title
Mast cells mediate malignant pleural effusion formation.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.
Publication Title
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 19 Downloadable Samples
- Illumina HiSeq 2500
Description
Early innate lymphoid progenitors (EILP) have recently been identified in the mouse adult bone marrow as a multipotential progenitor population committed to ILC lineages, but their relationship with other described ILC progenitors is still unclear. In this study, we examine the progenitor-successor relationships between EILP, IL-7R+ common lymphoid progenitors (ALP), and ILC precursors (ILCp). Bioinformatic, phenotypical, functional, and genetic approaches collectively establish EILP as an intermediate progenitor between ALP and ILCp. Our work additionally provides new candidate regulators of ILC development and clearly defines the stage of requirement of transcription factors key for early ILC development. Overall design: transcriptional profiling of early ILC progenitors (EILP, ILCp), and common lymphoid progenitors (ALP) was performed by RNA sequencing
Publication Title
Development and differentiation of early innate lymphoid progenitors.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
Description
Smyd3 is a histone methyltransferase implicated in tumorigenesis. Here we show that Smyd3 expression in mice is required but not sufficient for chemically induced liver and colon cancer formation. In these organs Smyd3 is functioning in the nucleus as a direct transcriptional activator of several key genes involved in cell proliferation, epithelial-mesenchymal transition, JAK/Stat3 oncogenic pathways, as well as of the c-myc and b-catenin oncogenes. Smyd3 specifically interacts with H3K4Me3-modified histone tails and is recruited to the core promoter regions of many but not all active genes. Smyd3 binding density on target genes positively correlates with increased RNA Pol-II density and transcriptional outputs. The results suggest that Smyd3 is an essential transcriptional potentiator of a multitude of cancer-related genes. Overall design: Standard Smyd3-deficient (Smyd3-KO) mice were generated using gene-trap ES cell clones (AS0527 from International Gene Trap Consortium), in which a selection cassette, containing the splice acceptor site from mouse EN2 exon 2 followed by the beta-galactosidase and neomycin resistance gene fusion gene and the SV40 polyadenylation sequence was inserted into the 5th intron of the Smyd3 gene. The resulting mice were devoid of Smyd3 mRNA and protein in all tissues, including liver and colon. For the generation of Smyd3-Tg mice the open reading frame of the mouse Smyd3 cDNA, which contained 3 Flag epitopes at the 3’ end was inserted into the StuI site of the pTTR1-ExV3 plasmid (Yan et al, 1990). The 6.8 kb HindIII fragment containing the mouse transthyretin enhancer/promoter, intron 1, Smyd3 cDNA, three Flag epitopes and SV40 poly-A site was used to microinject C57Bl/6 fertilized oocytes. Founder animals were identified by Southern blotting and crossed with F1 mice to generate lines. Specific overexpression in the liver was tested by RT-PCR analysis in different tissues.
Publication Title
Smyd3 Is a Transcriptional Potentiator of Multiple Cancer-Promoting Genes and Required for Liver and Colon Cancer Development.
Sample Metadata Fields
No sample metadata fields
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