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Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

ABSTRACT: p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231

ORGANISM(S): Homo sapiens

PROVIDER: GSE72009 | GEO | 2016/08/11

SECONDARY ACCESSION(S): PRJNA292709

REPOSITORIES: GEO

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Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231 p63 ChIP-SEQ on MCFDCIS and MDA-MB-231 cell lines

2016-08-11 | E-GEOD-72009 | biostudies-arrayexpress

Analysis of gene expression change due to knockdown of Slug expression in a basal-subtype breast cancer cell line, MCFDCIS.

Project description:Analysis of gene expression change due to knockdown of Slug expression in a basal-subtype breast cancer cell line, MCFDCIS. Total RNA isolated from MCFDCIS cells transfected with control or Slug specific siRNA.

2016-08-11 | E-GEOD-72011 | biostudies-arrayexpress

Analysis of gene expression change due to knockdown of Slug expression in a basal-subtype breast cancer cell line, MCFDCIS.

Project description:Analysis of gene expression change due to knockdown of Slug expression in a basal-subtype breast cancer cell line, MCFDCIS.

2016-08-11 | GSE72011 | GEO

Homo sapiens

Project description:Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

| PRJNA292709 | ENA

Isolation of subtype-specific N-Ras responsive genes in basal-like breast cancer cells

Project description:To identify the the N-Ras-controlled genes in basal-like cells, we used shRNA to repress N-RAS in basal-like SUM102PT, SUM149PT and claudin-low SUM159PT cells. We seek the genes regulated only in basal-like, but not in claudin-low cells, to isolate the genes controlled by N-Ras in a breast cancer subtype-specific fashion. We also overexpressed oncogenic form N-Ras(G12D) in these cells in order to compare the genes regulated by wild-type and oncogenic N-Ras. The shRNA silencing and overexpression were conducted by lentiviral infection in the cells, with non-silencing shRNA-infected cells as the controls. The infected cells were then selected in antibiotics for about 5 days before total RNAs were harvested for microarray analysis. N-Ras was silenced by shRNA or oncogenic N-Ras (G12D) was overexpressed in basal-like SUM102PT, SUM149PT and claudin-low SUM159PT cells.

2015-06-06 | E-GEOD-61768 | biostudies-arrayexpress

Isolation of subtype-specific N-Ras responsive genes in basal-like breast cancer cells

2015-06-06 | GSE61768 | GEO

Phenotypic and Molecular Characterization of the Claudin-low Intrinsic Subtype of Breast Cancer

Project description:In breast cancer, gene expression analyses have defined five tumor subtypes, each of which has unique biologic and prognostic features. Here, we characterize the recently identified claudin-low tumor subtype as showing low to absent expression of luminal differentiation markers, high enrichment for epithelial-to-mesenchymal transition markers, immune response genes, and cancer stem cell–like features. Clinically, most claudin-low tumors are poorprognosis estrogen receptor–negative, progesterone receptor–negative, and human epidermal growth factor receptor 2–negative (triple-negative) invasive ductal carcinomas with a high frequency of metaplastic and medullary differentiation. They also have a response rate to standard preoperative chemotherapy that is intermediate between that of basal-like and luminal tumors. Moreover, we show that a group of highly used breast cancer cell lines, and several genetically engineered mouse models, express the claudin-low phenotype. Finally, we confirm that a prognostically relevant differentiation hierarchy exists across all breast cancers in which the claudin-low subtype most closely resembles the mammary epithelial stem cell. These results should help to improve our understanding of the biologic heterogeneity of breast cancer and provide tools for the further evaluation of the unique biology of claudin-low tumors and cell lines.

2010-06-15 | GSE18229 | GEO

Expression data from ELK3 knocked down MDA-MB-231 cell line.

Project description:Triple-negative breast cancer is a highly aggressive tumor subtype that lacks effective therapeutic targets. Here, we show that ELK3 is overexpressed in a subset of breast cancers, in particular basal-like and normal-like/claudin-low cell lines. Suppression of ELK3 in MDA-MB-231 cells led to transdifferentiation from an invasive mesenchymal phenotype to a non-invasive epithelial phenotype both in vitro and in vivo. Suppression of ELK3 results in the extensive changes in genome expression profiles. Among these, GATA3, a master suppressor of metastasis, was epigenetically activated and we found that suppression of GATA3 led to the restoration of migration and invasion. These results suggest that the ELK3-GATA3 axis is a major pathway that promotes metastasis of MDA-MB-231 cells. Retrovirus expressing shRNA of ELK3 was transduced into MDA-MB-231 cell line and stable cell line of which ELK3 is suppressed more than 50% was selected by the drug selection (Puromycin).

2016-06-15 | E-GEOD-83325 | biostudies-arrayexpress

ChIP-seq of p63 and RNA-seq of knockdown and overexpression of p63

Project description:We performed ChIP-seq of p63 in ME-180 cell line and RNA-seq of knockdown and overexpression of p63

2019-08-06 | GSE135257 | GEO

Cell culture of p63 knock out and wild type bladder epithelial stem cell

Project description:Although there are several reports describing a stem cell fraction to form urothelium and lineage tracing studies in urinary bladder, it is still unclear about stem cells in mouse bladder epithelium. Here, we have established the cloning system of mouse stem cells from wild type and p63 knockout bladder. We isolated stem/progenitor cells from wild type and p63 knockout epithelium. From wild type bladder, we have cloned keratin 5-positive stem cells, and from p63 knockout epithelium, which loses basal cell fraction, we have cloned morphologically-distinct keratin 8 and claudin 3 positive stem cells, which may be reminiscent of intestinal metaplasia in bladder.

2015-10-01 | GSE68276 | GEO

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