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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE25620 | GEO | 2010/11/27

SECONDARY ACCESSION(S): PRJNA133967

REPOSITORIES: GEO

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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

Gene profile analysis of sorted Sca1+/cKit- BMCs obtained from young and aged mice bearing tumor or not

Project description:Sca1+/cKitâ hematopoietic BMCs of hosts bearing primary tumors promote the growth of distant tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from old mice bearing primary tumors lack this ability Sca1+/cKit- BMCs were isolated from young and old mice bearing Matrigel control or size-matched primary tumors by FACS directly into RLT Plus Buffer (Qiagen Rneasy Plus Micro Kit)

2016-07-21 | E-GEOD-74120 | biostudies-arrayexpress

Gene profile analysis of sorted Sca1+/cKit- BMCs obtained from young and aged mice bearing tumor or not

Project description:Sca1+/cKit– hematopoietic BMCs of hosts bearing primary tumors promote the growth of distant tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from old mice bearing primary tumors lack this ability

2016-07-21 | GSE74120 | GEO

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

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

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

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). Keywords: breast cancer, cell-of-origin, HMEC, BPEC,metastasis, tumor stem cells, tumor initiating cells, breast adenocarcinoma

2007-08-15 | GSE6885 | 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

Microarray-based gene expression data from BPLER tumor explants.

2013-07-02 | GSE48444 | GEO

HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [gene expression]

Project description:Heat-Shock Factor 1 (HSF1), master regulator of the heat-shock response, facilitates malignant transformation, cancer cell survival and proliferation in model systems. The common assumption is that these effects are mediated through regulation of heat-shock protein (HSP) expression. However, the transcriptional network that HSF1 coordinates directly in malignancy and its relationship to the heat-shock response have never been defined. By comparing cells with high and low malignant potential alongside their non-transformed counterparts, we identify an HSF1-regulated transcriptional program specific to highly malignant cells and distinct from heat shock. Cancer-specific genes in this program support oncogenic processes: cell-cycle regulation, signaling, metabolism, adhesion and translation. HSP genes are integral to this program, however, even these genes are uniquely regulated in malignancy. This HSF1 cancer program is active in breast, colon and lung tumors isolated directly from human patients and is strongly associated with metastasis and death. Thus, HSF1 rewires the transcriptome in tumorigenesis, with prognostic and therapeutic implications. We used microarrays to examine affect of HSF1 depletion on gene expression in cancer cell lines. Three cancer cell lines (BPLER, HMLER & MCF7) were transduced with either control shRNAi (Scramble or GFP) or an shRNAi that targets and depletes HSF1 (hA6). Another BPLER sample was subjected to a 1H, 42M-KM-^Z C heat shock. Two biological replicates for all samples.

2012-08-06 | E-GEOD-38232 | biostudies-arrayexpress