Exploration of the mechanisms underlying TNF-alpha resistance in breast cancer cells by a transcriptomic approach using an autophagy-dedicated microarray.
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Arnaud Muller
PROVIDER: E-MEXP-3074 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2012-03-06 | E-MEXP-3139 | biostudies-arrayexpress
Project description:We used DNA microarray technology to investigate the cytoskeleton gene expression profile associated with the acquisition of cell resistance to TNF-alpha in breast carcinoma cell line (MCF7) versus sensitive cells (1001).
2009-10-31 | E-MEXP-1927 | biostudies-arrayexpress
Project description:Gene expression profiling experiments were performed using the Agilent 44K whole human genome microarrays (Agilent Biotechnologies, Diegem, Belgium) according to the two-color gene expression analysis (Quick Amp labeling) protocol (version 5.7) from the manufacturer. Hybridizations were performed by comparing 300 ng of total RNA extracted from HEL cells treated with either 5 ?M of JI1 or 10 ?M of Erlotinib with that obtained from untreated cells. For each treatment, three biological replicates were analyzed in duplicate including a dye swap. Only high quality RNAs with a ribosomal RNA ratio greater than 1.9 and no evidence of degradation, as evaluated using the Agilent Bioanalyzer 2100 RNA 6000 nano assay, were used in this study. Microarray images were quantified using the GenePix Pro 6.1 software (Molecular Devices, Sunnyvale, CA, USA) as described in supplemental information.
2009-08-10 | E-MEXP-2244 | biostudies-arrayexpress
Project description:We have applied our research on a well-documented biological model, the epithelial cell evasion mediated by the ectopic expression of the snail protein. Indeed, ectopic expression of Snail, a transcriptional repressor, is widely used to study the initial step of epithelial cell evasion also called Epithelial to Mesenchymal Transition (EMT). During this process, cells loose their intercellular junctions and acquired motility and an invasive behaviour. In order to have a temporal view of the gene expression modulation that occurred during EMT, we have established a biological model based on the conditional expression of snail protein in human non-invasive MCF-7 breast carcinoma cells that do not express endogenous snail and exhibit a well-organized epithelial phenotype. 96 hours after snail induction, the epithelial to mesenchymal cell phenotype conversion is completed.
2009-01-06 | E-MEXP-1457 | biostudies-arrayexpress
Project description:To validate Actichip, we compared this microarray with two other well-established oligonucleotide-based platforms. We used 25-mer oligonucleotide commercial chips (Affymetrix, human genome U133A 2.0) and academic arrays prepared with a 70-mer oligonucleotide set (Operon, human whole genome version 2.0). The same series of high quality RNA samples purified from human breast adenocarcinoma MCF-7 cells and from human skeletal muscle was used in our experiments.
2007-06-01 | E-MEXP-968 | biostudies-arrayexpress
Project description:Candida albicans is a diploid fungal pathogen lacking a defined complete sexual cycle, and thus has been refractory to standard forward genetic analysis. Instead, transcription profiling and reverse genetic strategies based on Saccharomyces cerevisiae have typically been used to link genes to functions. To overcome restrictions inherent in such indirect approaches, we have investigated a forward genetic mutagenesis strategy based on the UAU1 technology. We screened 4700 random insertion mutants for defects in hyphal development, and linked two new genes (ARP2 and VPS52) to hyphal growth. Deleting ARP2 abolished hyphal formation, generated round and swollen yeast phase cells, disrupted cortical actin patches and blocked virulence in mice. The mutants also showed a global lack of induction of hyphae-specific genes upon the yeast-to-hyphae switch. Surprisingly, both arp2Î/Î and arp2Î/Îarp3Î/Î mutants were still able to endocytose FM4-64 and Lucifer Yellow, although as shown by time-lapse movies internalization of FM4-64 was somewhat delayed in mutant cells. Thus the non-essential role of the Arp2/3 complex discovered by forward genetic screening in C. albicans showed that uptake of membrane components from the plasma membrane to vacuolar structures is not dependent on this actin nucleating machinery. By forward genetic screening, we have identified genes that are essential for hyphal formation. One of the hits is the Arp2/3 complex, which is essential for hyphal formation, but not for viability in Candida albicans. To gain insights into cellular processes affected by disrupting Arp2/3 complex functions, we performed transcriptional profiling under yeast growth conditions (YPD at 30°C for three hours) or hyphal induction (YPD + 10% FBS at 37°C for three hours) and compared transcriptional consequences of deleting ARP2 to MYO5 and SLA2 microarray data sets (Oberholzer et al., 2006).
2010-10-08 | E-GEOD-19565 | biostudies-arrayexpress
Project description:Deleting components of the Arp2/3 complex in Candida albicans resulted in a global lack of hyphal specific gene induction. This observation suggests that the failure in hyphal growth of Arp2/3 complex mutants could be a result of failure to activate hyphal specific genes. If the hyphal defect was primarily due to failure to activate gene expression, de-repressing hyphal-specific gene expression by deleting the NRG1 repressor could potentially suppress the defect, as deletion of NRG1 leads to constitutive filamentous growth even in the absence of any hyphal induction signals (Garcia-Sanchez et al., 2005, Kadosh & Johnson, 2005). We therefore created an nrg1Î/Îarp2Î/Î mutant. When grown under non-inducing conditions, nrg1Î/Îarp2Î/Î cells showed the arp2Î/Î mutant morphology of round and swollen cells. When induced for hyphal growth, nrg1Î/Îarp2Î/Î cells also exhibited the arp2Î/Î cell morphology and did not form hyphae even after extended overnight incubation times. To determine if the hyphal-specific genes are de-repressed in the nrg1Î/Îarp2Î/Î mutant, we performed transcript profiling. We compared the nrg1Î/Îarp2Î/Î mutant grown under hyphal conditions to the arp2Î/Î mutant grown under the same conditions (10% serum, 37ï°C, three hours), and found that a significant number of hyphal-specific genes that are normally induced when WT cells are undergoing the yeast to hyphae switch (WT-HY) showed greater expression in the nrg1Î/Îarp2Î/Î mutant compared to arp2Î/Î cells (p-value 4.9x10-9). When we examined the set of NRG1-dependent hyphal-specific genes previously identified (Kadosh & Johnson, 2005), we found that seven of 28 genes (HYR1, SAP5, SAP4, KIP4, ORF19.6079, ALS3 and UME6) showed significantly increased expression (⥠2 fold) in nrg1Î/Îarp2Î/Î cells compared to arp2Î/Î cells, while a further four genes (IHD1, CBP1, ORF19.6705 and ALS10) showed moderately increased expression between 1.5 and 2-fold. Thus, while deleting a transcriptional repressor of the filamentation program leads to de-repression of many hyphal genes, the entire regulated gene set is not de-repressed; this presumably reflects the complex interplay that different transcriptional (co-) repressors exert on the yeast-to-hyphae transition (Garcia-Sanchez et al., 2005, Kadosh & Johnson, 2005). We further found that despite the increased induction of some hyphal genes in the nrg1Î/Îarp2Î/Î mutant, a few of those genes are not as highly induced as in WT cells. One gene that was induced in both the ânrg1Î/Îarp2Î/Î vs arp2Î/Îâ and the ânrg1Î/Îarp2Î/Î vs WTâ-comparisons is UME6, a recently identified key regulator of the hyphal program (Banerjee et al., 2008, Zeidler et al., 2009). Interestingly, although constitutive over-expression of UME6 in WT cells resulted in constitutive filamentous growth even in the absence of hyphae signals (Carlisle et al., 2009), the increased expression level of UME6 in the nrg1Î/Îarp2Î/Î mutant is not sufficient to restore filamentation in the absence of a functional Arp2/3 complex. Thus despite partial de-repression of the hyphal program, hyphae do not form, making it likely other roles of the Arp2/3 complex, such as its function in actin patch formation and actin branching, are required for hyphal development.
2010-01-22 | E-GEOD-19582 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE19565: Arp2/3 complex mutants show a pronounced lack of hyphal specific gene expression in Candida albicans GSE19582: Partial de-repression of the hyphal program does not restore hyphae formation in absence of a functional Arp2/3 complex Refer to individual Series
2010-05-15 | E-GEOD-19583 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE34255: Pho85, Pcl1, and Hms1 Signaling Governs Candida albicans Morphogenesis Induced by Elevated Temperature or Hsp90 Compromise [mRNA] GSE34938: Pho85, Pcl1, and Hms1 Signaling Governs Candida albicans Morphogenesis Induced by Elevated Temperature or Hsp90 Compromise [ChIP-chip] Refer to individual Series
2012-03-20 | E-GEOD-34939 | biostudies-arrayexpress
Project description:Mediator is an essential, evolutionarily conserved co-regulator of RNA polymerase II. Studies in model yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe showed remarkably conserved roles for Mediator despite high species divergence, and thus whether Mediator contributed to establishment of species-specific gene expression programs within related fungal species remains an open question. Here we show that in the fungal pathogen Candida albicans, the Mediator middle domain subunit Med31 has a conserved role with non-pathogenic model yeasts in regulation of Ace2-dependent cytokinesis genes and stress responses, but also additional roles in the transcription of genes associated with virulence traits: genes related to filamentous growth and gene families expanded in pathogenic vs non-pathogenic yeasts, such as the ALS adhesins and the FGR6 family of filamentous growth regulators. Consistently, Med31 is required for two key virulence attributes of C. albicans: filamentous growth and biofilm formation. Unlike our data in C. albicans, no role for Med31 in adhesin expression has been reported in model yeasts. To show biological relevance for the control over adhesin gene expression, we demonstrate that ALS1 is a relevant Med31 target for development of biofilms. Collectively, our data supports a role for Med31 in shaping species-specific gene expression in related fungal species. Two-color experimental design comparing cells with a ?med31 mutation with a control strain in which the MED31 gene was reintroduced. RNA from each replicate came from independent cultures.
2012-02-20 | E-GEOD-31632 | biostudies-arrayexpress