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Expression data in MDA-MB-231 cells treated with siATM, sip53 or control (SiNC) siRNA

ABSTRACT: Ataxia-telangiectasia mutated (ATM) protein kinase regulates the DNA damage response and is associated with cancer suppression. Here, we used microarray to study global transcriptomic expression to identify tumor-promoting functions of ATM.

ORGANISM(S): Homo sapiens

PROVIDER: GSE60479 | GEO | 2014/08/18

SECONDARY ACCESSION(S): PRJNA258379

REPOSITORIES: GEO

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Expression data in MDA-MB-231 cells treated with siATM, sip53 or control (SiNC) siRNA

Project description:Ataxia-telangiectasia mutated (ATM) protein kinase regulates the DNA damage response and is associated with cancer suppression. Here, we used microarray to study global transcriptomic expression to identify tumor-promoting functions of ATM. Human breast cancer MDA-MB-231 cells were transfected with siATM, sip53 or control siRNA followed by RNA extraction and hybridization on Affymetrix GeneChip Human Gene 2.0 ST array.

2014-08-18 | E-GEOD-60479 | biostudies-arrayexpress

Transcription profiling of ATM +/+, ATM +/- and ATM -/- human lymphoblastoid cell lines exposed to 5 Gy IR at 0, 4 and 24 hours to identify expression phenotypes in Ataxia Telangiectasia carriers and patients

Project description:Transcription profiling of ATM (Ataxia Telangiectasia Mutated) +/+ (Control), ATM +/- (AT Carrier) and ATM -/- (AT patient) human lymphoblastoid cell lines exposed to 5 Gy IR at 0, 4 and 24 hours to identify expression phenotypes in Ataxia Telangiectasia carriers and patients

2008-07-29 | E-TABM-321 | biostudies-arrayexpress

Expression data in MDA-MB-231 cells treated with siATM, sip53 or control (SiNC) siRNA

Project description: Not available

| S-ECPF-GEOD-60479 | biostudies-other

Reduced phosphorylated ATM expression is associated with poor prognosis and gemcitabine resistance in pancreatic cancer

Project description:Background & Aims: Loss of ataxia-telangiectasia mutated, occurring in patients with multiple primary malignancies, including pancreatic cancer, is associated with poor prognosis. This study investigated the detailed molecular mechanism through which ataxia-telangiectasia mutated expression affects the prognosis of pancreatic-cancer patients Methods: Ataxia-telangiectasia mutated and phosphorylated ataxia-telangiectasia mutated levels in pancreatic-cancer patients who underwent surgical resection were analyzed using immunohistochemistry staining. RNA sequencing was performed on ataxia-telangiectasia mutated-knockdown pancreatic-cancer cells to elucidate the mechanism underlying the involvement of ataxia-telangiectasia mutated in pancreatic cancer. Results: Immunohistochemical analysis showed that 15.3% and 27.8% of clinical samples had low levels of ataxia-telangiectasia mutated and phosphorylated ataxia-telangiectasia mutated, respectively. Low phosphorylated ataxia-telangiectasia mutated expression substantially reduced overall and disease-free survival in pancreatic-cancer patients. Loss of ataxia-telangiectasia mutated promoted MET and NTN1 over-expression via hypoxia-inducible factor-1α, thereby enhancing pancreatic-cancer cell proliferation and migration. Conclusions: These results demonstrate that the loss of ataxia-telangiectasia mutated activates downstream proto-oncogenes, inhibits apoptosis, and promotes tumor growth; moreover, loss of phosphorylated ataxia-telangiectasia mutated leads to poor prognosis in pancreatic-cancer patients. Thus, ataxia-telangiectasia mutated may serve as a potential molecular marker to monitor patient prognosis and as a potential target for pancreatic cancer therapy

2023-02-13 | GSE224882 | GEO

Transcription profiling of atm mutant, adm mutant and wild type whole plants and roots of Arabdiposis after gamma ray irradiation in a time series

Project description:Whole seedlings of wild type (4d) and atm mutants (4d) have been analyzed after a gamma ray irradiation of 0.75h, 1.5h, 3h & 5h (time course). Roots of wt (4d), atm (3d) and atr (4d) mutants have been analyzed after a 1h irradiation.<br><br> Ataxia Telangiectasia Mutated (ATM), encodes a large protein with a phosphatidylinositol 3-kinase (PI3K)-like domain at the C terminus (reviewed by Rotman and Shiloh, 1998). PI3K-related proteins make up a large family of Ser-Thr protein kinases, numerous members of which are involved in the regulation of cell cycle progression, responses to DNA damage, and the maintenance of genomic stability (Hoekstra, 1997). AtATM plays an essential role in meiosis and in the somatic response to DNA damage in plants, similar to the function of ATM in mammals and other eukaryotes.<br>Ataxia telangiectasia-mutated and Rad3-related (ATR) plays a central role in cell-cycle regulation, transmitting DNA damage signals to downstream effectors of cell-cycle progression.

2006-10-30 | E-MEXP-780 | biostudies-arrayexpress

Ataxia-telangiectasia cerebellar cortex expression

Project description:Cerebellar cortex expression in ataxia-telangiectasia patients and normal controls. The neurodegenerative disease known as ataxia-telangiectasia (A-T) is caused by the absence of the ATM (A-T mutated) protein. A long-standing mystery surrounding A-T is why cerebellar Purkinje cells (PCs) appear uniquely vulnerable to ATM-deficiency. Here, we present that 5-hydroxymethylcytosine (5hmC), a newly recognized epigenetic marker found at high levels in neurons, is substantially reduced in human A-T and Atm-/- mouse cerebellar PCs. TET1, an enzyme that converts 5mC to 5hmC, responds to DNA damage. Manipulation of TET1 activity directly affects neuronal cell cycle reentry and cell death after the induction of DNA damage. Quantitative, genome-wide analysis of 5hmC of samples from human cerebellum showed that in ATM-deficiency there is a remarkable genome-wide reduction of 5hmC enrichment at both proximal and distal regulatory elements. These results reveal a role of TET1-mediated 5hmC in DNA damage response, and provide insights into the basis of a PC-specific DNA demethylation alteration in ATM-deficiency. Human frozen tissue was obtained from the NICHD Brain and Tissue Bank of Developmental Disorders at the University of Maryland, Baltimore, MD. RNA was prepared and run on an Illumina Human HT-12 v4 microarray. 3 ataxia-telangiectasia (A-T) cases and 4 normal controls.

2015-10-30 | E-GEOD-61019 | biostudies-arrayexpress

Radiation-Induced DNA Damage and Repair Effects on 3D Genome Organization

Project description:We investigate the impact of DNA damage response and repair on 3D genome folding using Hi-C experiments on wild type cells and ataxia telangiectasia mutated (ATM) patient cells. Fibroblasts, lymphoblasts, and ATM-deficient fibroblasts were irradiated with 5 Gy X-rays and Hi-C was performed after 30 minutes, 24 hours, or 5 days after irradiation.

2020-09-04 | GSE136899 | GEO

Aspergillus nidulans: Control (0 h starvation) vs. induction of starvation (12 h and 24 h) for WT, delta xprG and delta atmA

Project description:Transcriptional profiling of A. nidulans comparing starvation for 0 (reference), 12 and 24 h. The main objective was to identify genes specifically regulated during starvation by atmA and xprG. The results of the experiment were further validated by real-time PCR. Experimental procedure: Three A. nidulans strains were used in this study: WT, delta atmA and delta xprG. Strains were grown on minimal medium for 24 h (0 h starvation reference), then exposed to 12 and 24 h starvation. atmA: ATM, Ataxia-Telangiectasia mutated; Malavazi, I., Savoldi, M., Da Silva Ferreira, M. E., Soriani, F. M., Bonato, P. S., De Souza Goldman, M. H. and Goldman, G. H. (2007), Transcriptome analysis of the Aspergillus nidulans AtmA (ATM, Ataxia-Telangiectasia mutated) null mutant. Molecular Microbiology, 66: 74-99 (PMID 17880424). xprG: extracellular protease; Margaret E. Katz, Karen-Ann Gray, Brian F. Cheetham, (2006) The Aspergillus nidulans xprG (phoG) gene encodes a putative transcriptional activator involved in the response to nutrient limitation, Fungal Genetics and Biology, 43, 190-199 (PMID 16464624).

2012-12-07 | E-GEOD-42732 | biostudies-arrayexpress

Effect of TERT and ATM on Gene Expression Profiles in Human Fibroblasts

Project description:Gene expression profiling was performed by use of serial analysis of gene expression (SAGE) on BJ normal human skin fibroblasts, A-T cells, and BJ and A-T cells transduced with hTERT cDNA and expressing telomerase activity. Keywords = telomere Keywords = telomerase Keywords = TERT Keywords = ataxia telangiectasia mutated Keywords = ATM Keywords = serial analysis of gene expression Keywords = SAGE Keywords = fibroblast Keywords: parallel sample

2004-01-16 | E-GEOD-953 | biostudies-arrayexpress

ATM regulates a DNA damage response post-transcriptional RNA operon in lymphocytes

Project description:Maintenance of genomic stability depends on the DNA damage response (DDR), a biological barrier in early stages of cancer development. Failure of this response results in genomic instability and high predisposition toward lymphoma, as seen in patients with ataxia-telangiectasia mutated (ATM) dysfunction. ATM activates multiple cell cycle checkpoints and DNA repair following DNA damage, but its influence on posttranscriptional gene expression has not been examined on a global level. We show that ionizing radiation (IR) modulates the dynamic association of the RNA-binding protein HuR with target mRNAs in an ATM-dependent manner, potentially coordinating the genotoxic response as an RNA operon. Pharmacologic ATM inhibition and use of ATM-null cells revealed a critical role for ATM in this process. Numerous mRNAs encoding cancer-related proteins were differentially associated with HuR depending on the functional state of ATM, in turn affecting expression of encoded proteins. The findings presented here reveal a previously unidentified role of ATM in controlling gene expression post-transcriptionally. Dysregulation of this DDR RNA operon is likely relevant to lymphoma development in ataxia-telangiectasia individuals. These novel RNA regulatory modules and genetic networks provide critical insight into the function of ATM in oncogenesis.

2011-01-05 | GSE25848 | GEO

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