Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA273955 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide analysis of DNA methylation in drug-tolerant cancer cell subpopulations
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Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
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Project description:Cancer relapse after curative treatment is thought to originate from drug-tolerant and invisible cancer cell subpopulations. Using cancer cell colonies emerging in the presence of drugs (drug-tolerant colonies, DTCs), we found that the drug-tolerant properties of DTCs are lost through a reversible mechanism. To examine whether epigenetic regulation is responsible for the phenotypic changes in DTCs, we performed a genome-wide analysis for relative CpG methylation between the DTCs and untreated colonies derived from MKN45 by NimbleGen Human Meth 385K Prom Plus CpG Arrays. Global changes in the methylation levels were evident in a chromosomal location-dependent manner. The methylation status of the upstream regions of the transcription start sites of the pluripotency-inducing genes showed good agreement with the qRT-PCR data. These results suggest that reversible drug-tolerant properties in DTCs are epigenetically regulated and associated with transcriptional regulation, including pluripotency-inducing factors. Comparison of untreated colonies v.s. DTCs derived from MKN45 cells.
2015-05-26 | E-GEOD-69203 | biostudies-arrayexpress
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Cancer relapse after curative treatment is thought to originate from drug-tolerant and invisible cancer cell subpopulations. Using cancer cell colonies emerging in the presence of drugs (drug-tolerant colonies, DTCs), we found that the drug-tolerant properties of DTCs are lost through a reversible mechanism. To examine whether epigenetic regulation is responsible for the phenotypic changes in DTCs, we performed a genome-wide analysis for relative CpG methylation between the DTCs and untreated colonies derived from MKN45 by NimbleGen Human Meth 385K Prom Plus CpG Arrays. Global changes in the methylation levels were evident in a chromosomal location-dependent manner. The methylation status of the upstream regions of the transcription start sites of the pluripotency-inducing genes showed good agreement with the qRT-PCR data. These results suggest that reversible drug-tolerant properties in DTCs are epigenetically regulated and associated with transcriptional regulation, including pluripotency-inducing factors.
2015-05-26 | GSE69203 | GEO
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression. Two-condition experiment, Normoxic MSCs vs. Hypoxic MSCs.
2011-02-19 | E-GEOD-20463 | biostudies-arrayexpress
Project description:Cancer relapse occurs even after curative treatment, suggesting the existence of undetectable cancer cell subpopulations and their drug-tolerant potential. We found that the number of drug-tolerant colonies (DTCs) was significantly suppressed by an RNA polymerase II (RNAPII) inhibitor, alpha-amanitin (alpha-AMA). To identify potential molecular target of alpha-AMA, we performed transcriptional profiling by Agilent-028004 SurePrint G3 Human GE 8x60K Microarray using untreated colonies and DTCs derived from MCF7. Among the top 2.5% of specifically induced genes in DTCs, we focused on TAF15 gene because its gene product binds RNAPII. A subsequent colony formation assay revealed that TAF15 knockdown suppressed the emergence of both DTCs and untreated colonies, suggesting that TAF15 is a crucial target of alpha-AMA in the context of DTC suppression.
2015-01-30 | GSE65419 | GEO
Project description:Cancer relapse occurs even after curative treatment, suggesting the existence of undetectable cancer cell subpopulations and their drug-tolerant potential. We found that the number of drug-tolerant colonies (DTCs) was significantly suppressed by an RNA polymerase II (RNAPII) inhibitor, alpha-amanitin (alpha-AMA). To identify potential molecular target of alpha-AMA, we performed transcriptional profiling by Agilent-028004 SurePrint G3 Human GE 8x60K Microarray using untreated colonies and DTCs derived from MCF7. Among the top 2.5% of specifically induced genes in DTCs, we focused on TAF15 gene because its gene product binds RNAPII. A subsequent colony formation assay revealed that TAF15 knockdown suppressed the emergence of both DTCs and untreated colonies, suggesting that TAF15 is a crucial target of alpha-AMA in the context of DTC suppression. Total RNA was extracted from two biological replicates of bulk untreated MCF7 colonies and MCF7 DTCs emerged in the presence of 0.8 µM CIS. For identification of the TAF15 gene, gene ontology analysis was performed using Database for Annotation, Visualization and Integrated Discovery (DAVID) software tools (http://david.abcc.ncifcrf.gov/).
2015-01-30 | E-GEOD-65419 | biostudies-arrayexpress
Project description:Targeted therapies require life-long treatment, as drug discontinuation invariably leads to tumor recurrence. Recurrence is thought to mainly be driven by minor subpopulations of drug tolerant persister (DTP) cells that survive the cytotoxic drug effect. In lung cancer, DTP studies have mainly been conducted using tumor cell line models.
2022-12-21 | GSE199716 | GEO
Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
2014-12-02 | GSE63741 | GEO