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Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [GEP data]

ABSTRACT: Copy number and Gene expression profiling of HT-29 wild-type and bortezomib resistant cell lines Identification of mechanisms of bortezomib resistance Gene expression differences between HT-29 cell line variants

ORGANISM(S): Homo sapiens

SUBMITTER: Jonathan Keats

PROVIDER: E-GEOD-29712 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [CGH data]

Project description:Copy number and Gene expression profiling of HT-29 wild-type and bortezomib resistant cell lines Identification of mechanisms of bortezomib resistance Copy number differences between HT-29 cell line variants and a HapMap control population of 9 female samples were identified using the Agilent 1M Human CGH microarray

2011-06-04 | E-GEOD-29711 | biostudies-arrayexpress

Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE29711: Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [CGH data] GSE29712: Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [GEP data] Refer to individual Series

2011-06-04 | E-GEOD-29713 | biostudies-arrayexpress

Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [GEP data]

Project description:Copy number and Gene expression profiling of HT-29 wild-type and bortezomib resistant cell lines Identification of mechanisms of bortezomib resistance

2011-06-04 | GSE29712 | GEO

Bortezomib resistance in THP-1 cell line

Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the THP-1 monocytic/macrophage cell line. On these subclones expression arrays were performed. We performed expression array three different bortezomib resistant subclones of the THP-1 cell line. The resistant subclones were spotted against the parental THP-1 wildtype cell line.

2008-06-14 | E-GEOD-11771 | biostudies-arrayexpress

Effect of polymeric formula on inflammation in intestinal epithelial cells

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2015-12-04 | E-GEOD-69605 | biostudies-arrayexpress

Bortezomib resistance in CCRF-CEM cell line [GEP]

Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed gene expression microarray analysis on four different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compaired to treated and untreated the parental CCRF-CEM wildtype cell line.

2015-11-04 | E-GEOD-74634 | biostudies-arrayexpress

RNA-seq analysis of HT-29, MCF10A, and MDA-MB-436 cells

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HT-29 cells treated with IFN-γ

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2013-08-06 | E-GEOD-38516 | biostudies-arrayexpress

Human colon cancer HT-29 and LS174T cells: stably transfected with shRNA-Ascl2/EGFP vs. stably transfected with shRNA-Control/EGFP

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2012-01-07 | E-GEOD-34926 | biostudies-arrayexpress

Mitochondria help avoid glucose addiction in cancer cells

Project description:Cancer cells consume large amounts of glucose because of their specific metabolic pathway. However, cancer cells exist in tumor tissue where glucose is insufficient. To survive, cancer cells likely have the mechanism to elude their glucose addiction. Here we show that functional mitochondria are essential if cancer cells are to avoid glucose addiction. Cancer cells with dysfunctional mitochondria, such as mitochondrial DNA-deficient rho0 cells and electron transport chain blocker-treated cells, were highly sensitive to glucose deprivation. Our data demonstrated that this sensitization was caused by failure of the unfolded protein response (UPR), an adaptive response mediated by the endoplasmic reticulum (ER). This study suggests a link between mitochondria and the ER during the UPR under glucose deprivation conditions and that mitochondria govern cell fate, not only through ATP production and apoptosis regulation but also through modulating the UPR for cell survival. Human cancer cell lines (HT-1080, HT-29, and mtDNA-deficient cells derived from these cell lines) were selected for RNA extraction and hybridization on Affymetrix microarrays. We examined the unfolded protein response (UPR), an adaptive response mediated by the endoplasmic reticulum (ER), of cancer cells under stress conditions. Abbreviations List: AA, antimycin A; Bu, buformin; Met, metformin; Phen, phenformin; Rot, rotenone; VST, versipelostatin; TM, tunicamycin; 2DG, 2-deoxyglucose; GS, glucose starvation. Capital S (_S) indicates the supernatant of sample including floating cells.

2010-05-28 | E-GEOD-16157 | biostudies-arrayexpress

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