Homo sapiens
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PROVIDER: PRJNA290403 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Development of colorectal cancer gene expression signatures from expression profiles of embryonic development, precancer progression and cancer samples
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Project description:To further development of our gene expression signature for survival prediction, we conducted expression profiles of embryonic development, precancer progression and cancer samples.
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Project description:To further development of our gene expression signature for survival prediction, we conducted expression profiles of embryonic development, precancer progression and cancer samples.
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Project description:This was a hypothesis generating experiment to look at miR expression in a range of oral keratinocytes, including normal, precancer and oral cancer samples. The cells were cultures as per standard protocols (duplicate cultures) before assessment on the Affy miRNA array (1.0) one normal oral keratinocyte, one precancer, and 2 cancer samples, all in duplicate
2013-11-28 | E-GEOD-52811 | biostudies-arrayexpress
Project description:Tumor-derived extracellular vesicles (TEVs) play a crucial role in cancer progression, metastasis and therapy resistance but their distinct profiles across different cancer stages and molecular subtypes remain underexplored. This study analyzed TEVs from epithelial (CMS2) and mesenchymal (CMS4) subtypes of colorectal cancer (CRC) using six cell lines and clinical samples. Investigation of the cargo of vesicles secreted by the two subtypes revealed significant differences in mRNA, miRNA, and protein profiles between the two subtypes. Notably, CMS2 predominantly secreted smaller, Tetraspanin-8 (TSPAN8) enriched EVs, while CMS4 produced both larger and smaller EVs, enriched in TSPAN4. This underscores the complexity of vesicle heterogeneity between these subtypes. Additionally, we assessed miRNA profiles from plasma-derived bulk TEVs in CRC patients.
2025-11-10 | PXD057149 | Pride
Project description:Goal of the experiment: To identify and understand the overall transcriptional programming of human colorectal cancer tumors by evaluating gene expression profiles of tumors from four murine models, and comparing and contrasting these to the developing stages of the mouse embryonic colon. Experiment description: Colorectal cancer results from multiple genetic and epigenetic events that produce variable histologies and clinical outcomes. To identify gene regulatory programs that underlie colon tumorigenesis, we profiled gene expression in 39 mouse colon tumors from four independent mouse models and compared this to mouse colon embryonic development, as well as with 100 human colon carcinomas. Here, we report a striking recapitulation of embryonic patterns of gene expression in both mouse and human colon tumors. All four of the mouse colon tumor models exhibited large-scale activation of embryonic gene expression signatures. The two nuclear beta-catenin-positive mouse tumors (azoxymethane-treated [AOM] and ApcMin/+), exhibited strong activation of genes characteristic of those expressed in the earliest embryonic stages, while tumors from two other models (Smad3-/- and Tgfb1-/- x Rag2-/-) exhibited lower activation of early stage-specific genes but substantial expression of general embryonic colon genes. Human colon cancer cases over-expressed genes characteristic of both early and late embryonic stages. Examining tumor gene expression through the lens of development has revealed an extensive network of therapeutic targets for cancer control. Keywords: Colorectal cancer, tumor, animal models, development, comparative genomics, orthologenome
2006-07-01 | GSE5206 | GEO
Project description:Expression data of miRNA profile from colorectal cancer and the adjacent normal tissues infected with F. nucleatum. Colorectal cancer(CRC) is among the most common cancer types in the world and one of the most lethal cancers. Fusobacterium nucleatum (F. nucleatum) plays an etiologic role in the development of colorectal cancer, but specific tumor molecules involved in the progression of CRC induced by F. nucleatum is not clear. This study investigated some miRNAs and the genes involved in the progression of F. nucleatum-induced colorectal cancer by Affymetrix miRNA microarray technology. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes between Colorectal cancer and the adjacent normal tissues (CONTROL) infected without F. nucleatum . The miRNA array was performed using the affymetrix GeneChip® miRNA 3.0 Array (Affymetrix, Santa Clara, California, United States). The chip was processed using a commercial Affymetrix array service (GeneTech Biotechnology Limited Company, Shanghai, China). The affymetrix GeneChip® miRNA 3.0 Array contains 2,999 probe sets unique to human, mouse and rat pre-miRNA hairpin sequences, 2,216 human snoRNA and scaRNA probe sets and covers 153 organisms (19,724 probe sets). Raw data sets were extracted from all Cel files (raw intensity file) after scanning of slides. These raw data sets were separately analyzed using Expression Console and GeneSpring GX12.5 software followed by differential miRNA expression, fold change & cluster analysis.
2018-11-06 | GSE122182 | GEO
Project description:Abnormal miRNA expression has been linked to the development and progression of human cancers, and such dysregulation can result from aberrant DNA methylation. We combined the analysis of miRNA expression data deposited with empirical DNA methylation data in HCT116 and DKO colon cancer cells (SRA accession# SRP001414) to identify novel DNA methylation regulated miRNAs. ABSTRACT: Abnormal microRNA (miRNA) expression has been linked to the development and progression of several human cancers, and such dysregulation can result from aberrant DNA methylation. While a small number of miRNAs is known to be regulated by DNA methylation, we postulated that such epigenetic regulation is more prevalent. By combining MBD-isolated Genome Sequencing (MiGS) to evaluate genome-wide DNA methylation patterns and microarray analysis to determine miRNA expression levels, we systematically searched for candidate miRNAs regulated by DNA methylation in colorectal cancer cell lines. We found 64 miRNAs to be robustly methylated in HCT116 cells and/or DNMT-1 and 3B doubleknock cells (DKO); eighteen of them were located in imprinting regions or already reported to be regulated by DNA methylation. In the remaining 46 miRNAs, expression levels of 18 were consistent with their DNA methylation status. Finally, 10 miRNAs were up-regulated by 5-aza-2'-deoxycytidine treatment and identified to be novel miRNAs regulated by DNA methylation. Moreover, we demonstrated the functional relevance of these epigenetically silenced miRNAs by ectopically expressing select candidates, which resulted in inhibition of growth and migration of cancer cells. Our study also provides a reliable strategy to identify DNA methylation-regulated miRNAs by combining DNA methylation profiles and expression data. [miRNA expression]: Total RNA was extracted from 3 biological replicate sets of HCT116 and DMNT-1 and 3B double knock out HCT116 (DKO) colorectal cancer cells.
2011-05-20 | E-GEOD-26819 | biostudies-arrayexpress
Project description:This was a hypothesis generating experiment to look at miR expression in a range of oral keratinocytes, including normal, precancer and oral cancer samples. The cells were cultures as per standard protocols (duplicate cultures) before assessment on the Affy miRNA array (1.0)
2013-11-28 | GSE52811 | GEO
Project description:Goal of the experiment: To identify and understand the overall transcriptional programming of human colorectal cancer tumors by evaluating gene expression profiles of tumors from four murine models, and comparing and contrasting these to the developing stages of the mouse embryonic colon. Experiment description: Colorectal cancer results from multiple genetic and epigenetic events that produce variable histologies and clinical outcomes. To identify gene regulatory programs that underlie colon tumorigenesis, we profiled gene expression in 39 mouse colon tumors from four independent mouse models and compared this to mouse colon embryonic development, as well as with 100 human colon carcinomas. Here, we report a striking recapitulation of embryonic patterns of gene expression in both mouse and human colon tumors. All four of the mouse colon tumor models exhibited large-scale activation of embryonic gene expression signatures. The two nuclear beta-catenin-positive mouse tumors (azoxymethane-treated [AOM] and ApcMin/+), exhibited strong activation of genes characteristic of those expressed in the earliest embryonic stages, while tumors from two other models (Smad3-/- and Tgfb1-/- x Rag2-/-) exhibited lower activation of early stage-specific genes but substantial expression of general embryonic colon genes. Human colon cancer cases over-expressed genes characteristic of both early and late embryonic stages. Examining tumor gene expression through the lens of development has revealed an extensive network of therapeutic targets for cancer control. Experiment Overall Design: Transcriptional signatures across human colorectal carcinomas and normal human colon tissue samples were evaluated by referencing all the samples to the median gene expression value across all the samples. A second complementary strategy compared the gene expression levels of the tumors to those of normal adult colon. Experiment Overall Design: Values were transformed from a log base 2 to linear values. Each measurement was divided by the 50.0th percentile of all measurements in that sample. Each gene was divided by the median of its measurements in all samples. If the median of the raw values was below 10 then each measurement for that gene was divided by 10 if the numerator was above 10, otherwise the measurement was thrown out.
2008-06-13 | E-GEOD-5206 | biostudies-arrayexpress