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Heparins treated human breast cancer MCF-7 cell

ABSTRACT: To inquire the a possible mechanism for heparin treatment improved cancer survival, three type of heparins: one standard heparin (unfractionated heparin (UFH), and two of low molecular weight heparin (LMWH) Fragmin and Clexane were used to treat cell for 24 hours. Total RNA was used for cDNA Microarray assay. Untreated cells were used as controls. Cell were treated by three type of heparins one standard heparin (unfractionated heparin (UFH), and two of low molecular weight heparin (LMWH) Fragmin and Clexane (40 IU/ml for each) were used to treat cell for 24 hours. Triplicate samples were prepared.

ORGANISM(S): Homo sapiens

SUBMITTER: Chen Yunliang Chen

PROVIDER: S-ECPF-GEOD-26537 | biostudies-other |

REPOSITORIES: biostudies-other

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Heparins treated human breast cancer MCF-7 cell

2011-01-11 | GSE26537 | GEO

Heparins treated human breast cancer MCF-7 cell

Project description:To inquire the a possible mechanism for heparin treatment improved cancer survival, three type of heparins: one standard heparin (unfractionated heparin (UFH), and two of low molecular weight heparin (LMWH) Fragmin and Clexane were used to treat cell for 24 hours. Total RNA was used for cDNA Microarray assay. Untreated cells were used as controls. Cell were treated by three type of heparins one standard heparin (unfractionated heparin (UFH), and two of low molecular weight heparin (LMWH) Fragmin and Clexane (40 IU/ml for each) were used to treat cell for 24 hours. Triplicate samples were prepared.

2011-01-11 | E-GEOD-26537 | biostudies-arrayexpress

Transcription profiling by array of human breast cancer cell line MCF-7 treated with estradiol

Project description:The Estrogen Receptor cofactors SRC1 (NCOA1, KAT13A), SRC2 (NCOA2, GRIP1, TIF2, KAT13C) , SRC3 (NCOA3, AIB1, KAT13B, Rac3) , CBP and p300 are assessed for their genome-wide chromatin binding capacities in the breast cancer cell line MCF7. To determine the Estrogen Receptor dependency of interactions, experiments were performed in the absence of hormone and after Estradiol treatment. In addition, the data were compared with Estrogen Receptor ChIP-seq data from the same timepoint of Estradiol treatment.

| S-ECPF-MTAB-788 | biostudies-other

Iron Chelators Treatment on MCF-7 Human Breast Cancer Cell

Project description:Iron-deficiency affects 500 million people, yet the molecular role of iron in gene expression remains poorly characterized. Moreover, the alterations in global gene expression after iron chelation remains unclear and are important to assess for understanding the molecular pathology of iron-deficiency and the biological effects of iron chelators. We assessed the effect on whole genome gene expression of two iron chelators (desferrioxamine and 2-hydroxy-1-napthylaldehyde isonicotinoyl hydrazone) that have markedly different permeability properties. Sixteen genes were significantly regulated by both chelators, while a further 50 genes were regulated by either ligand. Most of the genes identified in this study have not been previously described to be iron-regulated and are important for understanding the molecular and cellular effects of iron-deficiency. The MCF-7 cells were incubated with either control medium or this medium containing DFO (250 µM) or 311 (25 µM) for 24 h at 37oC. These concentrations were used since our previous studies demonstrated that under these conditions these chelators lead to up-regulation of iron-responsive genes such as the TfR1 after this incubation time.8 Moreover, the higher concentration of DFO was implemented due to its limited ability to permeate cell membranes. Total RNA was isolated from cells in 1 mL of TRIzol® reagent (Invitrogen). Samples were then prepared and hybridized to the Human Genome U133 Plus 2.0 430 2.0. The human GeneChip® U133 Plus 2.0 consists of greater than 47,000 transcripts and variants from over 38,500 well characterized human genes. On completion of hybridization and washing, microarray chips were scanned with the Affymetrix GeneChip® Scanner 3000 (Affymetrix).

| S-ECPF-GEOD-17832 | biostudies-other

Gene expression profiling and pathway analysis data in MCF-7 and MDA-MB-231 human breast cancer cell lines treated with dioscin.

Project description:Microarray technology (Human OneArray microarray, phylanxbiotech.com) was used to compare gene expression profiles of non-invasive MCF-7 and invasive MDA-MB-231 breast cancer cells exposed to dioscin (DS), a steroidal saponin isolated from the roots of wild yam, (Dioscorea villosa). Initially the differential expression of genes (DEG) was identified which was followed by pathway enrichment analysis (PEA). Of the genes queried on OneArray, we identified 4641 DEG changed between MCF-7 and MDA-MB-231 cells (vehicle-treated) with cut-off log2 |fold change|?1. Among these genes, 2439 genes were upregulated and 2002 were downregulated. DS exposure (2.30 ?M, 72 h) to these cells identified 801 (MCF-7) and 96 (MDA-MB-231) DEG that showed significant difference when compared with the untreated cells (p<0.05). Within these gene sets, DS was able to upregulate 395 genes and downregulate 406 genes in MCF-7 and upregulate 36 and downregulate 60 genes in MDA-MB-231 cells. Further comparison of DEG between MCF-7 and MDA-MB-231 cells exposed to DS identified 3626 DEG of which 1700 were upregulated and 1926 were down-regulated. Regarding to PEA, 12 canonical pathways were significantly altered between these two cell lines. However, there was no alteration in any of these pathways in MCF-7 cells, while in MDA-MB-231 cells only MAPK pathway showed significant alteration. When PEA comparison was made on DS exposed cells, it was observed that only 2 pathways were significantly affected. Further, we identified the shared DEG, which were targeted by DS and overlapped in both MCF-7 and MDA-MB-231 cells, by intersection analysis (Venn diagram). We found that 7 DEG were overlapped of which six are reported in the database. This data highlight the diverse gene networks and pathways in MCF-7 and MDA-MB-231 human breast cancer cell lines treated with dioscin.

| S-EPMC4905937 | biostudies-literature

Transcription profiling by array of human breast cancer MCF-7 cells treated with 17-AAG

Project description:17-AAG treatment of MCF-7 Microarray Files containing additional statistical analysis and data for meta-probesets are available on the FTP site for the experiment, in E-MTAB-339.additional.zip

| S-ECPF-MTAB-339 | biostudies-other

Human MCF-7 breast cancer cells: control vs. treated with conditioned medium of cancer associated adipose tissue

Project description:Transcriptional profiling of human MCF-7 breast cancer cells comparing MCF-7 cells treated with control medium (DMEM/F12 + 0,5% BSA) with MCF-7 cells treated with conditioned medium of cancer-associated adipose tissue (CMCAAT) obtained from 2 breast cancer patients. Goal was to determine the effects of CMCAAT treatment on global MCF-7 gene expression. Two-condition experiment: MCF-7 control vs. CMCAAT treated cells. Biological replicates: 3 control replicates pooled as 1 (LL 1-2-4), 4 CMCAAT replicates (LL 6, LL 8, LL 9, LL 10)

| S-ECPF-GEOD-58574 | biostudies-other

Piezo1 forms mechanosensitive ion channels in the human MCF-7 breast cancer cell line.

Project description:Mechanical interaction between cells - specifically distortion of tensional homeostasis-emerged as an important aspect of breast cancer genesis and progression. We investigated the biophysical characteristics of mechanosensitive ion channels (MSCs) in the malignant MCF-7 breast cancer cell line. MSCs turned out to be the most abundant ion channel species and could be activated by negative pressure at the outer side of the cell membrane in a saturable manner. Assessing single channel conductance (G?) for different monovalent cations revealed an increase in the succession: Li(+) < Na(+) < K(+) ?Rb(+) ? Cs(+). Divalent cations permeated also with the order: Ca(2+) < Ba(2+). Comparison of biophysical properties enabled us to identify MSCs in MCF-7 as ion channels formed by the Piezo1 protein. Using patch clamp technique no functional MSCs were observed in the benign MCF-10A mammary epithelial cell line. Blocking of MSCs by GsMTx-4 resulted in decreased motility of MCF-7, but not of MCF-10A cells, underscoring a possible role of Piezo1 in invasion and metastatic propagation. The role of Piezo1 in biology and progression of breast cancer is further substantiated by markedly reduced overall survival in patients with increased Piezo1 mRNA levels in the primary tumor.

| S-EPMC4322926 | biostudies-literature

MicroRNA-34a suppresses cell proliferation by targeting LMTK3 in human breast cancer mcf-7 cell line.

Project description:Breast cancer remains the leading cause of cancer mortality in females, and about 70% of the primary breast cancer patients are diagnosed ER?-positive, which is the most common type of breast cancer. MicroRNA-34a (miR-34a) has been shown to be a master regulator of tumor suppression in many types of cancers including breast cancer. However, the role of miR-34a in ER?-positive breast cancer has not been elucidated. Here, we find that in MCF-7, which is an ER?-positive breast cancer cell line, miR-34a is remarkably downregulated after E2 treatment. Overexpression of miR-34a by lentivirus suppresses cell proliferation, S phase ratio, and tumor formation in an E2-dependent manner in vitro. According to the mRNA sequence, lemur tyrosine kinase 3 (LMTK3), which is an important regulator of estrogen receptor alpha (ER?), is a predicted target of miR-34a. This is confirmed by dual luciferase reporter assay and the decrease of LMTK3 mRNA and protein levels after overexpression of miR-34a. Moreover, miR-34a overexpression decreases AKT signaling pathway and increases ER? phosphorylation status. Taken together, these results suggest that miR-34a inhibits breast cancer proliferation by targeting LMTK3 and might be used as an anti-ER? agent in breast cancer therapy.

| S-EPMC3864372 | biostudies-literature

Evidence of a genomic biomarker in normal human epithelial mammary cell line, MCF-10A, that is absent in the human breast cancer cell line, MCF-7.

Project description:This study investigated the use of DNA amplification fingerprinting (DAF) to identify biomarkers useful in the elucidating genetic factors that lead to carcinogenesis. The DNA amplification fingerprinting (DAF) technique was used to generate fingerprint profiles of a normal human mammary epithelial cell line (MCF-10A) and a human breast cancer cell line (MCF-7). When compared with one another, a polymorphic biomarker gene (262 base pairs (bps)) was identified in MCF-10A but was not present in MCF-7. This gene was cloned from the genomic DNA of the MCF-10A cell line, and subjected to Genbank database analysis. The analysis of the nucleotide sequence polymorphic marker (Genbank account: AC079630) shows that this biomarker has 100% homology with the nucleotide sequence of human chromosome 12 BAC RP11-476D10 (bps 19612-19353). The nucleotide sequence was used for possible protein translation product and the result obtained indicated that the gene codes for hypothetical protein XF2620. In order to evaluate the effects that the 262 bps biomarker would have on the morphology of MCF-7 cells, it was transfected into MCF-7 cells. There were observable changes in the morphology of the transfected cells. These changes included an increase in cell elongation and a decrease in cell aggregation.

| S-EPMC1510942 | biostudies-literature

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