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Transcription profiling by array of human DA-MB-231 breast cancer cells treated with various SCFA-hexosamine analogs

ABSTRACT: "The purpose of this study was to characterize the gene expression profile of MDA-MB-231 breast cancer cells treated with various SCFA-hexosamine analogs to better understand the role of various modifications to this scaffold. Experiment Overall Design: In total, six analogs were investigated in this study. For the relatively ""toxic"" C6-SCFA analogs, IC30 was selected to explore initial growth inhibitory and apoptotic gene expression changes. Two independent biological replicates were analyzed for each analog-treated condition. Three independent biological replicates were analyzed for the vehicle-treated control (EtOH)."

ORGANISM(S): Homo sapiens

SUBMITTER: Elmouelhi N

PROVIDER: S-ECPF-GEOD-11407 | biostudies-other | 2009 Apr

REPOSITORIES: biostudies-other

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Transcription profiling by array of human DA-MB-231 breast cancer cells treated with various SCFA-hexosamine analogs

Project description:The purpose of this study was to characterize the gene expression profile of MDA-MB-231 breast cancer cells treated with various SCFA-hexosamine analogs to better understand the role of various modifications to this scaffold. Experiment Overall Design: In total, six analogs were investigated in this study. For the relatively ""toxic"" C6-SCFA analogs, IC30 was selected to explore initial growth inhibitory and apoptotic gene expression changes. Two independent biological replicates were analyzed for each analog-treated condition. Three independent biological replicates were analyzed for the vehicle-treated control (EtOH).

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Project description:Parathyroid hormone-related protein (PTHrP) is overexpressed in many cancer types. This secretory protein can induce hypercalcaemia of malignancy by mimicking the action of calcium-regulating parathyroid hormone (PTH). PTHrP may also be involved in the regulation of migration, invasion, proliferation and apoptosis. It can either stimulate signal cascades, such as the cAMP pathway, or act on not yet defined targets in the nucleus. In this study, we analyzed the effect of PTHrP-specific siRNA on gene expression in MDA-MB-231 breast cancer cells. MDA-MB-231 cells were either transfected with the PTHrP-specific siRNA (siPTHrP) or a control siRNA (siLuc). Differences in gene expression pattern in siPTHrP- vs. siLuc-treated cells were measured by microarray analysis. More than 200 differentially expressed genes were found. Some of these genes have important functions in carcinogenesis. Experiment Overall Design: Three independent transfection experiments were performed. Cells were transfected with siPTHrP or siLuc by electroporation, grown for three days and harvested for isolation of total RNA. RNAs were subjected to microarray analysis. The RNAs of experiment 1 are designated as siLuc 1 and siPTHrP 1, those of experiment 2 as siLuc 2 and siPTHrP 2 etc.. To identify siPTHrP-responsive genes, the siPTHrP- and siLuc-RNAs of the same experiment were compared.

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Project description:Analogs of ManNAc, the committed precursor of sialic acid, decrease metastatic potential and trigger apoptosis in cancer cells. Adding Lev to ManNAc analogs increases their toxicity due to an ill-understood mechanism. Comparing gene expression profiles of cells treated with Ac4ManNLev and Ac4ManNAc will provide insight into the similarities and differences of these analogs. Specifically, MDA-MB-231 human breast cancer cells will be treated with Ac4ManNLev and Ac4ManNAc at doses that inhibit cell growth and induce the cell to undergo apoptosis later. RNA will be harvested in the early stage of cell arrest in order to identify genes altered by Ac4ManNLev and Ac4ManNAc. RNA preparations from three conditions, were sent to Microarray Core (E). One as control (Ethanol), and two experimental groups: high concentration Ac4ManNAc (100 uM) and high concentration Ac4ManNLev (100 uM). The aim is to gain insight into apoptosis and cell cycle arrest. Specifically, the Ac4ManNLev samples will be comprared to a less potent ManNAc analog. The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays.

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Project description:MiR-544 was inhibited by either a miR-544 antagomir or compound 1 under hypoxic conditions in MDA-MB-231 cells MiRNA microarray was utilized to examine the specificity of 1 for miR-544. 3 MDA-MB-231 samples treated with a miR-544 antagomir or compound 1 were subjected to hypoxia for a period of 5 days. After 5 days, samples were pooled and subjected to miRNA microarray analysis.

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Project description:From our previous data, we found that loss of ATAD3A gene expression in breast cancer cells results in loss of cell motility in vitro and metastasis in vivo. To obtain a better understanding of oncogenic pathway of ATAD3A, we have established the stable ATAD3A knockdown MDA-MB-231 cells using lentiviral strategy. We used the whole genome microarrays to detail the global programme of gene expression after depleting of ATAD3A and identified distinct classes of up or down-regulated metastmir associated with breast cancer cells migration Total RNA was extracted from ATAD3A stable knockdown cells (shATAD3A) and the control cells (shGFP). The labeled RNA was hybridized on U133 plus 2.0 Array. To identify altered gene expression patterns with or without ATAD3A expression, we compared average mRNA expression levels between the ATAD3A knockdown and control MDA-MB-231 cells.

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