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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.

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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

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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.

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

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