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Transformed Human Breast Epithelial Cell Types vs. Normal Cell-of-Origin

ABSTRACT: The gene expression of two different tumorigenic human breast epithelial cell types (HMLER and BPLER) is compared with their immortalized parental cell-of-origin (HME and BPE). Keywords: breast cancer, cell-of-origin, HMEC, BPEC,metastasis, tumor stem cells, tumor initiating cells, breast adenocarcinoma

ORGANISM(S): Homo sapiens

PROVIDER: GSE6885 | GEO | 2007/08/15

SECONDARY ACCESSION(S): PRJNA98559

REPOSITORIES: GEO

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Transcription profiling of human breast tumor epithelia cell types HMLER and BPLER compared to immortalized parent cells of origin - HME and BPE

Project description:The gene expression of two different tumorigenic human breast epithelial cell types (HMLER and BPLER) is compared with their immortalized parental cell-of-origin (HME and BPE). Experiment Overall Design: Two different normal primary human mammary epithelial cell populations (BPECs and HMECs) were isolated based on their differing in vitro growth requirements. These cells were immortalized by hTERT giving rise to BPE and HME cells. These hTERT immortalized cells (BPE and HME) were transformed by SV40-early region (LT+st) and H-Ras giving rise to transformed tumorigenic derivatives BPLER and HMLER. Biological replicates (4 - 6 samples) for each of 4 cell types were analyzed (untransformed hTERT immortalized cell populations (BPE&HME), and transformed tumorigenic derivatives (BPLER & HMLER).

2008-06-15 | E-GEOD-6885 | biostudies-arrayexpress

Next Generation Sequencing and differential expression analysis in stem-like vs. non-stem breast cancer cells in response to HDAC1 and HDAC7 knockdown

Project description:Purpose: We performed RNA-seq differential expression analysis after 72h HDAC1 and HDAC7 knockdown in order to evaluate the transcriptional regulation exerted by HDAC1 and HDAC7 in a stem-like (BPLER) vs. non-stem (HMLER) breast cancer (BrCa) cell model (please search for keywords "BPLER" or "HMLER" in GEO to access over 240 associated data sets). Results: HDAC7 knockdown by a pool of siRNAs resulted in altered expression of nearly three times the genes in BPLER vs. HMLER cells (2545 vs. 763), with the two cell types sharing altered expression of 328 genes. In stem-like BPLER cells, HDAC7 knockdown caused significant alterations in gene expression (1068 down and 1477 up). Fewer genes, less than half of BPLER, were altered in non-stem HMLER cells (448 down and 315 up), with 199 repressed and 129 activated genes shared between the two cell types. In contrast, 72h HDAC1 knockdown resulted in nearly equal numbers of altered genes in BPLER vs. HMLER cells (3187 vs. 2627), with the two cell types sharing altered expression of 637 genes. Moreover, the number of repressed (1570 vs. 1307) and activated (1617 vs. 1320) gene transcripts was similar in the two cell types In HMLER cells, HDAC7 knockdown resulted in alterations of significantly fewer gene transcripts compared to HDAC1 knockdown (508 vs. 2681), in both repressed (305 vs. 1362) and activated (203 vs. 1319) transcripts. Conclusions: Cumulatively, these results highlight that HDAC7 regulates nearly three times as many genes in stem-like compared to non-stem BrCa cells. In contrast, HDAC1 regulates equal number of genes in the same cell context, suggesting a predominant association of HDAC7 with the cancer stem cell phenotype.

2020-02-24 | GSE131631 | GEO

Microarray-based gene expression data from BPLER tumor explants.

2013-07-02 | GSE48444 | GEO

Gene profile analysis of sorted Sca1+/cKit- BMCs obtain from mice bearing instigator, non-instigator and Matrigel

2010-11-27 | GSE25620 | GEO

Microarray-based gene expression data from BPLER tumor explants.

Project description:The gene expression of 6 different mouse xenografts initiated by BPLER cells analyzed by microarray. Basal-like triple negative breast cancers (TNBC) have poor prognosis. To study the basal-like transcriptional profile of tumors transformed by defined genetic elements, the human breast epithelial cell line BPLER was injected into NOD/SCID mice. The resulting tumors were excised for expression analysis. Keywords: breast cancer, BPLER, metastasis, tumor stem cells, tumor initiating cells, breast adenocarcinoma BPLER cells were derived from human primary breast epithelial cells propagated in WIT medium (Ince et al, Cancer Cell, 2007). These cells were transformed with hTERT, SV40 early region and hRASV12 by retroviral transduction. BPLER have a TNBC-like phenotype in vitro and are highly enriched for tumor-initiating cells. To define the phenotype of BPLER-derived tumors in vivo, BPLER cells were injected in the mammary fat-pad of 6 NOD/SCID mice. Once tumors were palpable, mice were sacrificed and tumors excised. Total RNA was extracted using Trizol. The gene expression profile of each tumor was assessed by mRNA microarray analysis. Based on histology and principal component analysis of microarray data, BPLER tumors were remarkably similar to human primary TNBC encountered in the clinic (Petrocca et al, Cancer Cell, 2013).

2013-07-02 | E-GEOD-48444 | biostudies-arrayexpress

Genome-wide analysis of the RNA polyemerase I trascription factor UBF1/2 binding in mouse and human cell lines.

Project description:We report ChIP-Seq analysis of the RNA polyemerase I trascription factor UBF1/2 in NIH3T3, HMEC and HMLER cell lines. NIH3T3* samples: We correlated UBF1/2 binding across the genome with that of RNA polemerase I (Pol I), RNA polemerase II (Pol II) and chromatin states in NIH3T3 cells We perfromed ChIP-seq of UBF1/2 (2 biological replicates), Pol I (POLR1A/RPA194), Pol II, H3K9me3, H3K4Me3, H3K9ac, H4 hyperacetylation and genomic DNA input as reference. HMEC* samples: We report ChIP-Seq analysis of UBF1/2 and Pol I (POLR1A/RPA194) in human mammary epithelial cells (HMEC). In addition we include UBF1/2 ChIP-seq in the tumourigenic epithelial cell line HMLER. In this study, we compared UBF1/2 binding in HMEC to UBF1/2 binding in in the tumorigenic HMLER cells, an isogenic HMEC-derived cell line expressing the SV40 large-T, TERT, and an oncogenic allele of the HRAS gene (expressing HRASV12G) that forms tumors in nude mice (Elenbaas et al., Gene & Development 2001) We sequenced UBF1/2 ChIP and Pol I(POLR1A/RPA194) ChIP and gDNA input from HMEC. We sequenced UBF1/2 ChIP and gDNA input from HMLER

2014-11-14 | E-GEOD-63255 | biostudies-arrayexpress

Genome-wide analysis of the RNA polyemerase I trascription factor UBF1/2 binding in mouse and human cell lines.

Project description:We report ChIP-Seq analysis of the RNA polyemerase I trascription factor UBF1/2 in NIH3T3, HMEC and HMLER cell lines.

2014-11-14 | GSE63255 | GEO

Gene profile analysis of sorted Sca1+/cKit- BMCs obtain from mice bearing instigator, non-instigator and Matrigel

Project description:Sca1+/cKit– hematopoietic BMCs of hosts bearing instigating tumors (BPLER) promote the growth of responding (HMLER-HR) tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from mice bearing Non-instigating tumors lack this ability Sca1+/cKit- BMCs were isolated from mice bearing Matrigel control or size-matched instigating or non-instigating tumors by FACS directly into Trizol reagent (Invitrogen).

2010-11-27 | E-GEOD-25620 | biostudies-arrayexpress

Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (2)

Project description:DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. RNAseq of untreated HMEC-hTERT cells, siCtrl, siMBD2 or DAC treated HMLER cells, siCtrl or siMBD2 treated HME-ZEB1-RAS and HME-shP53-RAS cells, in duplicates.

2015-06-17 | E-GEOD-63234 | biostudies-arrayexpress

Aberrant DNA methylation of miRNA genes in breast cancer

Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of the study was to determine how is DNA methylation of miRNA genes changed in breast cancer cell lines an breast tumor specimens. Breast cancer cell lines vs. HMEC. Breast tumor tissue specimens vs. non-tumor tissue specimens. Biological replicates: 12 breast tumor specimens, 5 breast non-tumor specimens, 7 breast cancer cell lines, 3 HMEC genotypes, 3 HMF genotypes. Immunoprecipitation using anti-Methylcytosine (5MeC) antibody.

2012-05-25 | E-GEOD-38254 | biostudies-arrayexpress

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