Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data of MCF-7 cells treated with gamma tocotrienol (g-T3)

ABSTRACT: Gamma tocotrienol induces apoptosis in breast cancer cells however, the molecular mechanisms are not completely understood. We used microarrays to detail the global programme of gene expression underlying the effects of gamma tocotrienols on MCF-7 cells and identified distinct classes of up-regulated genes during this process. MCF-7 cells were grown in DMEM medium with 5% FBS. The cells were treated with vehicle control (DMSO) or 40 uM of gamma tocotrienol for 24 h for RNA extraction and hybridization on Affymetrix microarrays. Four independent experiments were performed.

ORGANISM(S): Homo sapiens

SUBMITTER: Habtom Ressom

PROVIDER: E-GEOD-21946 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gamma-tocotrienol induced apoptosis is associated with unfolded protein response in human breast cancer cells.

Patacsil Dorrelyn D Tran Anh Thu AT Cho Youn Sook YS Suy Simeng S Saenz Francisco F Malyukova Irina I Ressom Habtom H Collins Sean P SP Clarke Robert R Kumar Deepak D

The Journal of nutritional biochemistry 20110322 1

Gamma-tocotrienol (γ-T3) is a member of the vitamin E family. Tocotrienols (T3s) are powerful antioxidants and possess anticancer, neuroprotective and cholesterol-lowering properties. Tocotrienols inhibit the growth of various cancer cell lines without affecting normal cells. Less is known about the exact mechanisms of action of T3s on cell death and other growth inhibitory pathways. In the present study, we demonstrate that γ-T3 induces apoptosis in MDA-MB 231 and MCF-7 breast cancer cells as e ...[more]

PMID: 21429729

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Project description:Interferon-gamma (IFN-gamma) is approved as a drug to treat chronic granulomatous disease and osteopetrosis and is also used in hyperimmunoglobulin E syndromes. These primary immunodeficiencies involve defects in neutrophils/polymorphonuclear cells. Neutrophils mature in the bone marrow and then enter the blood where they quickly undergo apoptotic cell death with a half-life of 5-10 hours. Therefore we reasoned that IFN-gamma might exert its effects on neutrophils via prolonged exposure to cells undergoing maturation toward a terminally differentiated state in the marrow rather than by its brief exposure to short-lived circulating cells. To explore this possibility we made use of PLB-985 cells which are a myeloblast-like myeloid cell line that can be differentiated into a mature, neutrophil-like state by treatment with various agents including DMSO. In initial studies we investigated transcription and protein expression in PLB-985 cells undergoing DMSO-mediated maturation in the presence or absence of IFN-gamma and identified several classes of immunity related genes that were differentially expressed in the presence of the drug and could potentially explain the immune supportive properties of IFN-gamma. Next we explored if the effect of IFN-gamma on expression of these genes is dependent on whether the cells are undergoing maturation; to do this we compared the effects of IFN-gamma on cells cultured with and without DMSO. For a subset of genes the expression level changes caused by IFN-gamma were much greater in maturing cells than non-maturing cells. These findings indicate that developmental changes associated with cell maturation can modulate the effects of IFN-gamma and supports our hypothesis that the effects of the drug on developing neutrophils in the bone marrow may be very different from its effects on mature cells in the blood. We also compared the effects on gene expression of applying IFN-gamma either during DMSO mediated PLB-985 cell maturation or after maturation i.e. IFN-gamma was applied to already mature cells. For some genes we found that IFN-gamma applied to mature cells caused large changes in expression similar to those seen when IFN-gamma was applied during maturation, however for other genes no effect was seen when drug was applied to mature cells but large effects were seen when drug was applied during DMSO treatment. This data suggests that, in the former class of genes, the effects of IFN-gamma application during maturation are largely the result of the effects of the drug on cells approaching full maturity but in the latter class of genes the effects of IFN-gamma only become apparent when it is present throughout maturation. This further supports our hypothesis that the effects of IFN-gamma are modulated by developmental changes associated with cell maturation.

Dataset Information

Expression data of MCF-7 cells treated with gamma tocotrienol (g-T3)

Publications

Gamma-tocotrienol induced apoptosis is associated with unfolded protein response in human breast cancer cells.

Similar Datasets

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