E-MTAB-6275
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6275 | ExpressionAtlas | 2019-08-30
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-6275-analysis-methods.tsv | Tabular | |||
| E-MTAB-6275-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-6275-configuration.xml | Xml | |||
| E-MTAB-6275-percentile-ranks.tsv | Tabular | |||
| E-MTAB-6275.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:Expression profiling in four human bladder cancer cell lines
2025-01-23 | E-MTAB-2610 | ExpressionAtlas
Project description:In order to understand the contribution of autophagy and alternative NF-kappaB signalling to transcriptional output in A549 lung cancer cells, RNAi was used to knockdown the expression of core autophagy genes (ATG5, ULK1) or the key subunit of alternative NF-kappaB RELB. Seven samples were prepared for each biological replicate; two sequence independent non-targeting control siRNAs were transfected as a negative control. Three sequence independent siRNAs targeting the core autophagy machinery were transfected (ATG5 si, ATG5 si(2), ULK1 si). N.B. ATG5 si(2) only partially ablates Atg5 protein expression whereas ATG si has greater efficacy. Two sequence independent siRNAs targeting RELB were transfected (RELB si, RELB si(2) ). Three independent biological replicates of all conditions were obtained, by performance of the experiment on different days.
2015-09-18 | E-GEOD-73158 | biostudies-arrayexpress
Project description:Autophagy plays an important role in physiology and tumorigenesis. We and others have demonstrated that Ha-ras overexpression induces autophagy in NIH3T3 cells. Autophagic machinery is regulated by a family of autophagy associated genes (Atg). The inducible Ha-ras oncogene was introduced into mouse embryo fibroblast Atg5 wild type [MEF-Atg5(+/+)] and Atg5 knock-out [MEF-Atg5(-/-)] cells and the stable cell lines MR and M5R were established, respectively. Our results showed that M5R cell induced larger tumor formation compared with MR cells while these two cell lines were subcutaneously injected into SCID mice under Ha-ras overexpression conditions. It indicates that Atg5 is involved in the suppression of Ras-related tumor formation. MicroRNA (miRNA), approximately 22 nucleotide of non-coding RNA, regulates transcription and translation of the target genes and is involved in cell differentiation and tumorigenesis. A miRNA microarray (932 probes) screening was conducted to identify the autophagy-tumorigenesis-related miRNAs. Among the significant genes, miR-224 was highly expressed in autophagy deficient cell and it induced tumors. Overexpression miR-224 enhanced the activity of migration and invasion in vitro and tumor formation in vivo. In conclusion, this is the first report to demonstrate that autophagy suppresses tumor formation through down-regulation of microRNA in this case miR-224. MR and M5R cell lines were treated with IPTG for 48 hr. In addition, these cell lines were subcutaneously injected into mice to induce tumor formation. The RNA samples were extracted from above cell lines and tumors. In this research, BEL/ITRI 15K V1.0 miRNA microarray chips were used to evaluate the miRNA expression profile.
2012-06-25 | E-GEOD-38911 | biostudies-arrayexpress
Project description:We used proteomic profiling to identify proteins in the mTOR-autophagy axis. Mouse cell lines lacking individual autophagy genes (Atg5 or Ulk1/Ulk2) were treated with an mTOR inhibitor to induce autophagy and cultured in media with either glucose or galactose. Mass spectrometry proteome profiling revealed an elevation of both known autophagy proteins and candidates for new autophagy components.
2020-01-23 | PXD014990 | Pride
Project description:Autophagy is activated in pancreatic ductal adenocarcinoma (PDAC) and is currently being considered a promising therapeutic target in clinical trials. PDAC is a highly lethal disease with incidence rate equalling mortality rate. Main reasons for PDAC lethality are late-stage diagnosis, high agressiveness and metastatic rate, lack of effective treatments as well as specific diagnostic markers. Here we show that varying levels of the Autophagy related gene 5 (Atg5) determine pancreatic tumor formation and malignancy. While homozygous deletion of Atg5 blocks tumor progression in an in vivo model of PDAC, heterozygous deletion increases tumor aggressiveness and metastasis. Further analyses reveal that monoallelic loss of Atg5 affects mitochondrial homeostasis, changes intracellular calcium oscillations, heightens extracellular cathepsin activities , and promotes a pro-tumorigenic inflammatory microenvironment collectively enhancing tumor cell migration, invasion, and metastasis. Future treatments should take into account that variations in the autophagy pathway may have opposing effects on pancreatic tumor load, especially considering the multitude of autophagy inhibitors currently tested in clinical trials.
2018-10-15 | E-MTAB-6275 | biostudies-arrayexpress
Project description:Transcriptional profiling by array of bone marrow and peripheral blood samples from patients with cytogenetically normal acute myeloid leukemia to study gene expression profiles associated with different levels of miR-3151 expression
2025-01-23 | E-MTAB-1075 | ExpressionAtlas
Project description:To explore the mechanisms of autophagy in the regulation of vascular tumour cells, we generated three autophagy-related genes, Fip200, Atg5 and Atg7, knockout vascular tumor cells in 562 cell line by CRISPR-Cas9-based sgRNAs. Three independent replicates of mRNA samples were prepared from each KO cells and subjected to RNA-sequencing in comparison to three samples from control 562 cells. We examined changes in gene expression by transcriptional profiling of Fip200 KO, Atg5 KO, and Atg7 KO cells, compared to control 562 cells respectively.
2023-01-12 | GSE193568 | GEO
Project description:Transcriptional profiling by array of lymphoblastoid cell lines (LCLs) from six DS and six euploid individuals to investigate differential gene expression and pathway deregulation associated with trisomy 21
2025-01-23 | E-MTAB-1238 | ExpressionAtlas
Project description:Autophagy plays an important role in physiology and tumorigenesis. We and others have demonstrated that Ha-ras overexpression induces autophagy in NIH3T3 cells. Autophagic machinery is regulated by a family of autophagy associated genes (Atg). The inducible Ha-ras oncogene was introduced into mouse embryo fibroblast Atg5 wild type [MEF-Atg5(+/+)] and Atg5 knock-out [MEF-Atg5(-/-)] cells and the stable cell lines MR and M5R were established, respectively. Our results showed that M5R cell induced larger tumor formation compared with MR cells while these two cell lines were subcutaneously injected into SCID mice under Ha-ras overexpression conditions. It indicates that Atg5 is involved in the suppression of Ras-related tumor formation. MicroRNA (miRNA), approximately 22 nucleotide of non-coding RNA, regulates transcription and translation of the target genes and is involved in cell differentiation and tumorigenesis. A miRNA microarray (932 probes) screening was conducted to identify the autophagy-tumorigenesis-related miRNAs. Among the significant genes, miR-224 was highly expressed in autophagy deficient cell and it induced tumors. Overexpression miR-224 enhanced the activity of migration and invasion in vitro and tumor formation in vivo. In conclusion, this is the first report to demonstrate that autophagy suppresses tumor formation through down-regulation of microRNA in this case miR-224.
2012-06-26 | GSE38911 | GEO
Project description:miRNA expression of 6h EBSS treatment induced autophagy in Atg5 WT and KO mouse embryonic fibroblasts (MEF) were examined. For the 1st comparison, the control group is Atg5 WT MEF without EBSS treatment, the experiment group is Atg5 KO MEF without EBSS treatment; For the 2nd comparison, the control group is Atg5 WT MEF without EBSS treatment, the experiment group is Atg5 WT MEF with 6h EBSS treatment; For the 3rd comparison, the control group is Atg5 WT MEF with 6h EBSS treatment, the experiment group is Atg5 KO MEF with 6h EBSS treatment.The PIQORTM Analyzer were used for the analysis.
2011-11-21 | E-MTAB-880 | biostudies-arrayexpress