Gene expression profiles in human oral squamous cell carcinoma tissues and cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Koh-ichi Nakashiro
PROVIDER: E-GEOD-36090 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2011-09-01 | E-MEXP-3299 | biostudies-arrayexpress
Project description:Global gene expression analysis was performed on a panel of 23 osteosarcoma samples of primary and metastatic origin using the Applied Biosystems Gene Expression Array System. When comparing the primary tumours with the metastases, we found a significantly increased expression of genes involved in immunological processes, e.g. coding for cytokines and chemokines, in the metastatic samples, suggesting that these signal molecules play an important role in promoting metastasis. In addition, a comparison of the gene expression in primary samples from patients with or without metastases demonstrated that patients who later developed metastases had high expression of the chemokine (C-X-C motif) receptor 4 (CXCR4), similar to the metastatic samples. Increased knowledge of mechanisms and interactions between specified molecular signalling pathways in osteosarcomas could lead to a more rational strategy for development of targeted therapy. Total RNA was isolated from tumor tissue of osteosarcoma patients. Gene expression patterns of metastatic versus primary samples were compared, as well as primary samples from patients who did or did not later develop metastases.
2012-01-01 | E-GEOD-32981 | biostudies-arrayexpress
Project description:The number of vertebrae is strictly defined for any given species1, and depends on the number of somites, which are periodically formed as perfectly matched cell masses during mid-embryogenesis, where the somite segmentation clock prescribes the timing2. The tempo of the clock is affected by surrounding condition, despite which the same number of somites is formed3, suggesting that the clock may be tunable to adapt to the environmental condition. Here, we demonstrate a tunability of the segmentation clock in the period depending on the level of Notch signaling that senses the surrounding information to adjust the number of somites and vertebrae precisely, in which we propose a mechanism of the clock with a feedback loop of Notch signaling by Notch-regulated ankyrin repeat protein (Nrarp). Disruption of Nrarp in mouse resulted in the loss of two vertebrae, due to 4-min extension of the period of the clock elicited by the up-regulation of Notch activity, whereas pharmacological diminishment of Notch activity shortens it by a few min. The Notch inhibitor rescues the phenotype of Nrarp knockout mice in the period. These results are comprehended by mathematical analyses, in which the period of the clock is fine-tuned by Notch activity that Nrarp adjusts. Overall, our results are the first to provide molecular evidence of fine-tuning of the segmentation clock that preserves the number of somites and vertebrae. Nrarp mutant mouse which have LacZ gene instead of Nrarp coding region was generated by homologous recombinant. Fragnant female heterozygous mutant mice, mated with heterozygous mutant male, were dissected at embryonic day 10.5 (E10.5). 12 PSMs were collected in each genotype to extract total RNA.
2010-10-01 | E-GEOD-18419 | biostudies-arrayexpress
Project description:The decision of metazoan cells to live or undergo programmed cell death hinges on the balance between the levels of pro- versus anti-apoptotic gene products. The general RNA polymerase II (Pol II) transcription factor, TFIID, plays a central role in the regulation of gene expression through its core promoter recognition and co-activator functions. The core TFIID subunit TAF6 is a co-activator for the pro-apoptotic p53 tumour suppressor protein. Our previous studies identified a specialized isoform of TAF6, termed TAF6 that can specifically be induced in apoptosis. To elucidate the impact of TAF6 on gene expression and cell death, we employed modified antisense oligonucleotides to enforce expression of endogenous TAF6. The induction of endogenous TAF6 triggered apoptosis in several cancer cell lines. Importantly, TAF6 also induces apoptosis in tumor cell lines devoid of p53, placing TAF6 function downstream of p53. Microarray experiments uncovered a TAF6-induced transcriptome landscape displaying enhanced expression of genes of the Notch, oxidative stress, integrin, p53 and apoptosis pathways. Our data show that the TAF6 pathway is a pivotal signalling nexus that controls pro-apoptotic gene expression programs. Keywords: Treatment with splice site switching antisense oligonucleotides, induction of apoptosis Biological triplicates, 3 conditions: control oligonucleotide, Taf6 oligonucleotide, specificity control Bcl-x oligonucleotide
2010-11-27 | E-GEOD-8752 | biostudies-arrayexpress
Project description:Renal ischemia reperfusion injury (I/R) has great clinical relevance and many treatments and hospitalizations are associated with this pathological process. Animal models are widely used in the development of kidney I/R studies and numerous papers have been published in this field in recent years suggesting that the nature of the animal species used in these models can lead to a different response to ischemic insult. The Brown Norway (BN) rat strain is known to show endogenous resistance to the ischemic process and several studies have sought to identify the cell mechanism present in this resistance. Despite of all the previously reported works, little is know about the genetic response of BN in front of ischemic insult. By means of a microarray comparative genetic study between BN and the ischemia susceptible rat strain Sprague Dawley (SD), the present work determine the genetic response to the I/R process in both rat strains and the genes that are differentially expressed during the I/R process and link them with some of the main cytoprotective processes responsible for the endogenous resistance to renal ischemic injury in BN rats. The following experimental groups for BN and SD rats (n=3 per group) were studied: Group 1: Control (C): Animals subjected to identical maneuvers as the I/R group except that the renal pedicles were not clamped. Group 2: Ischemia/Reperfusion (I/R): Animals were subjected to 45 min of bilateral ischemia and 24 h of reperfusion. Gene expression profiles were obtained from control and I/R groups in the two rat strains in three biological replicates, resulting in 12 hybridizations from 2 groups × 2 strains × 3biological replicates. To evaluate the technical reliability of microarrays, replicate microarrays were performed on several RNA samples. In total, 12 hybridizations were performed for this study.
2007-12-27 | E-GEOD-9943 | biostudies-arrayexpress
Project description:Background The complete sequencing of the human genome and its subsequent analysis revealed a predominant role for alternative splicing in the generation of proteome diversity. Splice switching oligonucleotides (SSOs) are a powerful and specific tool to experimentally control alternative splicing of endogenous messenger RNAs in living cells. SSOs also have therapeutic potential to treat diseases that are caused by aberrant splicing. The assignment of biological roles to alternative splicing events of currently unknown function promises to provide a largely untapped source of potential new therapeutic targets. Here we have developed a protocol that combines high sensitivity microarrays with the transfection of SSOs to monitor global changes in gene expression downstream of alternate, endogenous splice events. Findings When applied to a well-characterized splicing event in the Bcl-x gene, the application of high sensitivity microarrays revealed a link between the induction of the Bcl-xS isoform and the repression of genes involved in protein synthesis. Conclusions The strategy introduced herein provides a useful approach to define the biological impact of any given alternative splicing event on global gene expression patterns. Furthermore, our data provide the first link between Bcl-xS expression and the repression of ribosomal protein gene expression. Biological triplicates, 2 conditions: control oligonucleotide, Bcl-x oligonucleotide
2008-10-02 | E-GEOD-9851 | biostudies-arrayexpress
Project description:Follicular thyroid tumours were investigated using global gene expression analysis. Aim of this study was the identification of new markers for follicular thyroid carcinoma. Keywords: cell type comparison Gene expression analysis of 4 follicular thyroid adenomas, 4 follicular thyroid carcinomas, and 4 microinvasive follicular thyroid carcinomas.
2009-02-27 | E-GEOD-15045 | biostudies-arrayexpress
Project description:To elucidate the impact of TAF6d on cell death and gene expression, here we have employed modified antisense oligonucleotides to enforce expression of endogenous TAF6d. The induction of endogenous TAF6d triggered apoptosis in tumor cell lines, including cells devoid of p53. Microarray experiments revealed that TAF6d activates gene expression independently of cellular p53 status. Our data define TAF6d as a pivotal node in a signaling pathway that acts immediately downstream of p53 to control gene expression programmes and apoptosis. Keywords: Treatment with splice site switching antisense oligonucleotides, induction of apoptosis Biological triplicates, 4 conditions: isogenic p53+/+ and -/- cells; control oligonucleotide, TAF6 AS2 oligonucleotide
2008-06-26 | E-GEOD-10795 | biostudies-arrayexpress
Project description:Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53R273H in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53R273H targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin. For the study of the consequences of mutant p53 (R273H) knockdown on gene expression, total RNA from parental U251 glioblastoma cells and UsiA12 clone was prepared from two independent cell culture experiments (biological replicates) and processed for microarray-based profiling of gene expression. UsiA12 clone was derived from the U251 cells transfected with the pSuper-p53 and pCI-neo vectors.
2010-06-24 | E-GEOD-13991 | biostudies-arrayexpress
Project description:The aim was to analyze the expression of genes in T cell clones having different functional profiles (Th1, Th0, Th17, Th2) obtained from the same individual. Keywords: Gene expression, T cell clones, Th17 characterisation The T cell clones were derived according to well known protocol, using different cytokines, and classified on the basis of their ability to produce cytokines. Once characterized for their production of IL-4, IL-12, gamma-IFN, IL-13, IL-1, they were used to prepare microarray experiments.
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