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Hypoxia response by human breast cancer cell MDA-MB-231 sublines

ABSTRACT: Two MDA-MB-231 sublines, SCP2 and LM2 (4175), were applied to low oxygen (1%) for 0, 6 and 24 hours, then profiled for RNA expression. Two sublines, each sublines has three conditions: 0h, 6h and 24h for hypoxia treatment. Each condition has two repeats. Total 12 samples

ORGANISM(S): Homo sapiens

SUBMITTER: Yibin Kang

PROVIDER: E-GEOD-17188 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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In vivo dynamics and distinct functions of hypoxia in primary tumor growth and organotropic metastasis of breast cancer.

Lu Xin X Yan Carol H CH Yuan Min M Wei Yong Y Hu Guohong G Kang Yibin Y

Cancer research 20100504 10

Tumor hypoxia is known to activate angiogenesis, anaerobic glycolysis, invasion, and metastasis. However, a comparative analysis of the potentially distinct functions of hypoxia in primary tumor growth and organ-specific metastasis has not been reported. Here, we show distinct hypoxia kinetics in tumors generated by the MDA-MB-231 breast cancer sublines with characteristically different primary tumor growth rates and organotropic metastasis potentials. Hypoxia-induced angiogenesis promotes both ...[more]

PMID: 20442288

Similar Datasets

Hypoxia response by human breast cancer cell MDA-MB-231 sublines

Project description:Two MDA-MB-231 sublines, SCP2 and LM2 (4175), were applied to low oxygen (1%) for 0, 6 and 24 hours, then profiled for RNA expression.

2010-06-07 | GSE17188 | GEO

Global changes in gene expression in response to miR-200 overexpression in 4TO7 cells

Project description:Transcriptional profiling of 4TO7 cells stably overexpressing miR-200s or CDH1. We observe a dramatic shift in the gene signatures when miR-200s (cluster 2; miR-200c/141, or both clusters) are overexpressed relative to controls. However, cluster 1 overexpression (miRs-200b/a/429) alone or CDH1 overexpression does not induce global changes in gene expression to levels observed for cluster 2 (miR-200c/141) or both clusters together. One cell line (4TO7) cells: four different overexpression experiments, Cluster 1, Cluster 2, Clusters 1+2, CDH1, and respective controls, Puro vec, Hygro vec, Puro+Hygro vec and Puro vec. Each experiment has two biological replicates. Total, 16 samples.

2010-12-23 | E-GEOD-19631 | biostudies-arrayexpress

Tumor-derived Jagged1- and Notch-dependent transcription changes in MC3T3-E1 osteoblasts

Project description:Transcriptional profiling of MC3T3-E1 osteoblasts that were flow cytometry-separated from cocultures with control or Jagged1-overexpressing tumor cells and treated with either DMSO control or 1μM MRK-003 (gamma-secretase inhibitor). One cell line (MC3T3-E1) cells: four different experimental conditions: cultured with (1) control tumor cells + DMSO; (2) Jagged1-overexpressing tumor cells + DMSO; (3) control tumor cells + MRK-003; (4) Jagged1-overexpressing tumor cells + MRK-003. Each experiment has two biological replicates. Total, 8 samples.

2010-08-15 | E-GEOD-20517 | biostudies-arrayexpress

VCAM1 promotes outbreak from dormant bone metastasis

Project description:A weakly bone metastatic variant of the breast cancer cell line MDA-MB-231, SCP6, gave rise to highly bone metastatic sublines (PD1, PD2A-E) after long time dormancy in vivo. These cell lines were subjected to microarray analysis with data drawn from previous studies (Kang et al., 2003; Minn et al. 2005; Lu and Kang 2009; Lu and Kang 2010). Keywords: Cell type comparison 12 cell lines (parental MDA-MB-231 with biological repeats; weakly bone metastasis variants: SCP3, SCP4 and SCP6; post-dormancy sublines of SCP6: PD1, PD2A, PD2B, PD2C, PD2D, PD2E and PD2R) were cultured and subjected to Affymetrix microarray analysis. Data were analysed with Genespring software.

2011-01-30 | E-GEOD-20611 | biostudies-arrayexpress

Global gene expression of Ruegeria pomeroyi strain DSS3 in response to glucose, ammonium, phosphate, or sulfate limitation

Project description:We used the previously designed oligonucleotide-based microarray (Burgmann et al. Environmental Microbiology 2007, 9: 2742-2755) to detect the transcripts of R. pomeroyi DSS-3 genes when the cells were cultured under steady-state carbon (glucose), nitrogen (ammonium), phosphorus (phosphate), or sulfur (sulfate) limitation. A total of 14 mRNA samples were hybridized to the arrays (three biological replicates from glucose, ammonium, phosphate, or sulfate limitation and one technical replicate each for ammonium or sulfate limitation)

2011-09-30 | E-GEOD-27032 | biostudies-arrayexpress

Enhancement of metastasis by spontaneous ploidy doubling of breast cancer cell MDA-MB-231.

Project description:MDA-MB-231 bone-metastatic subline 1833 and lung metastatic subline 4175 underwent spontaneous ploidy doubling in culture, i.e. the genome approximately duplicated itself gradually. The modal- and hyper-ploid subpopulations during the ploidy transition were sorted into two separate sublines, 1833-Modal and 1833-Hyper for 1833, 4175-Modal and 4175-Hyper for 4175. Their expresssion patterns were compared to each other as well as to other MDA-MB-231 sublines isolated previously by Kang et al. 2003 and Minn et al. 2005. Keywords: Cell type comparison 19 cell lines were analyzed, including the parental line MDA-MB-231, modal-ploid sublines 1833-Modal and 4175-Modal, hyper-ploid sublines 1833-Hyper and 4175-Hyper, strongly bone-metastatic lines 1833 (the original subline after short culture), 2274, 2268 and 2269, weakly bone-metastatic lines 2293, 2295 and 2297, strongly lung-metastaic lines 4142, 4173, 4175 (the original subline after short culture) and 4180, and weakly lung-metastatic lines SCP6, SCP21 and SCP26. Single sample for each line.

2010-06-08 | E-GEOD-16554 | biostudies-arrayexpress

RNA sequencing of Normal Human Fibroblasts and Patient Fibroblasts with Novel SCP2 Variant

Project description:The purpose of this study was to identify differentially expressed genes beween normal and SCP2 mutant fibroblasts

2022-07-05 | GSE199634 | GEO

Bypass mechanisms of the AR pathway in castration-resistant PC346 prostate cancer cells

Project description:Prostate cancer is initially dependent on androgens for survival and growth, making hormonal therapy the cornerstone treatment for invasive tumors. However, despite initial remission, the cancer will inevitably recur. The present study was set to investigate how androgen-dependent prostate cancer cells eventually survive and resume growth under androgen-deprived and antiandrogen supplemented conditions Microarray technology was used to analyze differences in gene expression between androgen-responsive and hormone-refractory prostate cancer cell lines. As model system, we used the androgen-responsive PC346C cells and its castration-resistant sublines: PC346DCC, PC346Flu1 and PC346Flu2. These sublines were derived from the parental PC346C by long-term androgen ablation (PC346DCC), supplemented with the antiandrogen hydroxyflutamide (PC346Flu1 and PC346Flu2). Previous studies revealed distinct AR modifications in all three castration-resistant sublines: AR overexpression (PC346Flu1), AR down-regulation (PC346DCC) and T877A AR mutation (PC346Flu2). Each of the hormone-refractory sublines were cultured in their respective selection medium (steroid-stripped medium for PC346DCC, supplemented with 1 mM OH-Flutamide for PC346Flu1 and Flu2) and hybridized on the microarrays, together with the parental androgen-responsive PC346C (cultured in complete medium supplemented with 0.1 nM R1881). To account for the biological variability and dye-preferential binding to oligonucleotides on the microarray, four replicate arrays were performed per cell line, using two independent cell passages in dye-swap.

2010-10-21 | E-GEOD-21596 | biostudies-arrayexpress

Antiestrogen-resistant subclones of MCF-7 human breast cancer cells are derived from a common clonal drug-resistant progenitor

Project description:Emergence of antiestrogen-resistant cells in MCF-7 cells during suppression of estrogen signaling is a widely accepted model of acquired breast cancer resistance to endocrine therapy. To obtain insight into the genomic basis of endocrine therapy resistance, we characterized MCF-7 monoclonal sublines that survived 21-day exposure to tamoxifen (T-series sublines) or fulvestrant (F-series sublines) and sublines unselected by drugs (U-series). All T/F-sublines were resistant to the cytocidal effects of both tamoxifen and fulvestrant. However, their responses to the cytostatic effects of fulvestrant varied greatly, and their remarkably diversified morphology showed no correlation with drug resistance. mRNA expression profiles of the U-sublines differed significantly from those of the T/F-sublines, whose transcriptomal responsiveness to fulvestrant was largely lost. A set of genes strongly expressed in the U-sublines successfully predicted metastasis-free survival of breast cancer patients. Most T/F-sublines shared highly homogeneous genomic DNA aberration patterns that were distinct from those of the U-sublines. Genomic DNA of the U-sublines harbored many aberrations that were not found in the T/F-sublines. These results suggest that the T/F-sublines are derived from a common monoclonal progenitor that lost transcriptomal responsiveness to antiestrogens as a consequence of genetic abnormalities many population doublings ago, not from the antiestrogen-sensitive cells in the same culture during the exposure to antiestrogens. Thus, the apparent acquisition of antiestrogen resistance by MCF-7 cells reflects selection of preexisting drug-resistant subpopulations without involving changes in individual cells. Our results suggest the importance of clonal selection in endocrine therapy resistance of breast cancer.

2009-08-27 | GSE14986 | GEO

Chromosome 20 Aberrations at the Diploid-Aneuploid Transition in Sporadic Colorectal Cancer

Project description:DNA aneuploid sublines in sporadic colorectal cancers (CRCs) are quite frequent (about 85%) and likely the consequence of chromosomal instability and DNA copy number aberrations (CNAs). In order to gain insight into the mechanisms of the diploid-aneuploid transition in CRCs, we compared the CNA status in both diploid and aneuploid sublines. We used fresh/frozen material from 17 aneuploid CRCs, which was separated into 17 DNA diploid and 17 aneuploid sublines using enrichment of the epithelial component by multiparameter flow cytometry and sorting. CNA status of both sublines was obtained by array comparative genomic hybridization. The DNA diploid sublines from the aneuploid CRCs showed already CNAs, in particular, gains at 20p and 20q. The same aberrations were detected at increased frequencies in the corresponding DNA aneuploid sublines. Moreover, the very frequent gains/losses of chromosomes 4, 7, 8, 13, 15, and 18 in the DNA aneuploid sublines were absent or rare in the DNA diploid sublines from the same sporadic aneuploid CRCs. The comparison of the DNA diploid and aneuploid sublines from aneuploid CRCs suggests that 20p and 20q gains may play a role in the diploid-aneuploid transition. The 20q chromosomal arm appears of particular interest since it harbors several genes implicated in chromosomal instability.

2014-10-20 | GSE47148 | GEO

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