Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeted disruption of the BCL9/beta-catenin complex in cancer

ABSTRACT: Stabilized Alpha-Helix peptides of BCL9 HD2 (SAH-BCL9) block BCL9 and B9L interactions with beta-catenin and specifically downregulate Wnt target gene expression. RNA from triplicate SAH-BCL9B- and vehicle-treated DLD1 samples (10 µM each for 12 hours) was hybridized to Affymetrix Human U133 Plus 2.0 arrays to asses global gene expression changes.

ORGANISM(S): Homo sapiens

SUBMITTER: Madeleine Lemieux

PROVIDER: E-GEOD-33143 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Targeted disruption of the BCL9/β-catenin complex inhibits oncogenic Wnt signaling.

Takada Kohichi K Zhu Di D Bird Gregory H GH Sukhdeo Kumar K Zhao Jian-Jun JJ Mani Mala M Lemieux Madeleine M Carrasco Daniel E DE Ryan Jeremy J Horst David D Fulciniti Mariateresa M Munshi Nikhil C NC Xu Wenqing W Kung Andrew L AL Shivdasani Ramesh A RA Walensky Loren D LD Carrasco Daniel Ruben DR

Science translational medicine 20120801 148

Deregulated Wnt/β-catenin signaling underlies the pathogenesis of a broad range of human cancers, yet the development of targeted therapies to disrupt the resulting aberrant transcription has proved difficult because the pathway comprises large protein interaction surfaces and regulates many homeostatic functions. Therefore, we have directed our efforts toward blocking the interaction of β-catenin with B cell lymphoma 9 (BCL9), a co-activator for β-catenin-mediated transcription that is highly e ...[more]

PMID: 22914623

Similar Datasets

Targeted disruption of the BCL9/beta-catenin complex in cancer

Project description:Stabilized Alpha-Helix peptides of BCL9 HD2 (SAH-BCL9) block BCL9 and B9L interactions with beta-catenin and specifically downregulate Wnt target gene expression.

2012-08-23 | GSE33143 | GEO

The specific interactions of Bcl9/Bcl9L with b-catenin and Pygopus promote breast cancer growth, invasion and metastasis

Project description:Summary: We studied how the binding of beta-catenin to the transcriptional coactivators B-cell CLL/lymphoma 9 (Bcl9) and Bcl9-Like (Bcl9L) affected mammary gland carcinogenesis in the MMTV-PyMT transgenic mouse model of metastatic breast cancer. Conditional knockout of both Bcl9 and Bcl9L resulted into tumor cell death. In contrast, disrupting the interaction of Bcl9/Bcl9L with beta-catenin, either by deletion of their HD2 domains or by a point mutation in the N-terminal domain of beta-catenin (D164A), diminished primary tumor growth and tumor cell proliferation and reduced tumor cell invasion and lung metastasis. In comparison, the effect of disrupting the HD1 domain-mediated binding of Bcl9/Bcl9L to Pygopus was more moderate. Interfering with the beta-catenin - Bcl9/Bcl9L - Pygo chain of adaptors only partially impaired the transcriptional response of mammary tumor cells to Wnt3a and TGF-beta treatment. The results indicate that Bcl9/Bcl9L critically enforce canonical Wnt signaling in its contribution to breast cancer growth and malignant progression.

2021-08-20 | GSE182404 | GEO

DLD1

Project description:DLD1 is an APC mut, KRAS mut, P53 mut CRC cell line. PROX1 transcription factor, target of Wnt pathway in CRC, is our protein of interest.DLD1 cells are PROX1 negative. We overexpressed through lentiviral expression PROX1 protein or the empty vector psd44, through selection of the cells in puromycin resistance. Afterwards we compared the transcriptional program of the DLD1-PROX1 and DLD1-Control cells growing in monolayer in vitro.

2014-09-18 | E-MTAB-2020 | biostudies-arrayexpress

Mouse ameloblasts Bcl9 interactors

Project description:Bcl9 and Bcl9l (Bcl9l) are commonly thought as beta-catenin-dependent Wnt signaling transcriptional activators. We find however that, in the enamel-producin ameloblasts cells, Bcl9/9l are localiyed in the cytoplasm toward to apical secretory membrane. We performed pull down followed by mass spectrometry analysis to discover the molecular partners of Bcl9 that could explain this cytoplasmic localyzation.

2017-02-13 | PXD005449 | Pride

Gene expression in DCIS.COM with BCL9 knockdown

Project description:There is limited research on which specific Wnt targets are regulated by B-Cell Lymphoma-9 (BCL9) and whether BCL9 regulates other signaling pathways to drive cancer malignancy. Here we demonstrated that BCL9 drives DCIS invasive progression by regulation of genes involved in cellular growth, invasion and migration.

2020-01-17 | GSE143790 | GEO

Beta-catenin target genes in colorectal carcinoma cell lines with deregulated Wnt/beta-catenin signaling

Project description:To validate the suitability of two commonly used colorectal cancer cell lines, DLD1 and SW480, as model systems to study colorectal carcinogenesis, we treated these cell lines with beta-catenin siRNA and identified beta-catenin target genes using DNA microarrays. The list of identified target genes was compared to previously published beta-catenin target genes found in the PubMed and the GEO databases. Based on the large number of beta-catenin target genes found to be similarly regulated in DLD1, SW480 and LS174T as well as the large overlap with confirmed β-catenin target genes, we conclude that DLD1 and SW480 colon carcinoma cell lines are suitable model systems to study beta-catenin regulated genes and signaling pathways 12 arrays (2 cell lines, 2 treatments, 3 biological replicates)

2013-12-31 | E-GEOD-44097 | biostudies-arrayexpress

BCL9/STAT3 Regulation of Transcriptional Enhancer Networks Promote DCIS Progression

Project description:There is limited research on which specific Wnt targets are regulated by B-Cell Lymphoma-9 (BCL9) and whether BCL9 regulates other signaling pathways to drive cancer malignancy. Here, using ChIP-Exo we have demonstrated that BCL9 in a protein complex with STAT3 drives DCIS invasive progression by regulation of enhancers and enhancer associated target genes involved in cellular growth, invasion and migration.

2020-01-09 | GSE143313 | GEO

Gene expression induced by 5SA-Atoh1 in DLD1 cells

Project description:To investigate the function of Atoh1 in colon cancer cells. We have employed whole genome microarray expression profiling as a discovery platform to iedntify the gene expression induced by Atoh1 in colon cancer cells. Mutated Atoh1 (5SA-Atoh1) replaced 5 serine residues to Alanin for the protein stabilization were expressed in human colon cancer cellline; DLD1 cells. Triplicated RNAs were generated from GFP expressing DLD1 cells and 5SA-Atoh1 expressing DLD1 cell, respectively.

2012-04-10 | E-GEOD-37143 | biostudies-arrayexpress

Pull down of full length and mutant BCL9 (deltaHD1) in mouse colorectal tumors and colonic epithelium

Project description:Bcl9 and Bcl9l (Bcl9l) are commonly thought as beta-catenin-dependent Wnt signaling transcriptional activators. Here we searched for BCL9 interacts that could explain the PYGO-independent phenotype induced be the loss of the HD1 (PYGO-binding) domain of BCL9

2020-08-10 | PXD018805 | Pride

ChIP-seq experiment of the beta-catenin co-factor Bcl9 in developing forelimbs.

Project description:We isolated ca. 500 forelimbs at 10 days post coitum, and performed ChIP-seq using anti-Bcl9 antibodies. Bcl9 is a beta-catenin transcriptional cofactor, therefore it allows the identification of binding sites of the canonical Wnt signalling-dependent transcriptional complex. This experiment allowed to define that, in this developmental context, Bcl9 acts as a beta-catenin dedicated partner. Moreover, it established a series of genome-wide Bcl9 (therefore Wnt/beta-catenin) tissue-specific target loci, thereby assessing the genetic relationship existing between Wnt signaling and other signalling cascades (e.g. the Bmp pathway).

2019-02-21 | E-MTAB-7652 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data