C-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Stefano Sioletic
PROVIDER: E-GEOD-57531 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We assayed the effect of c-Jun overexpression on gene expression in the three DDLPS cell lines using RNA-Seq (Illumina). 141, LPS12 and 510 has been overexpressed with c-Jun or control c-DNA and results were analyzed in high-througput sequencing metadata.
2014-06-30 | E-GEOD-57530 | biostudies-arrayexpress
Project description:Affymetrix exon arrays to identify genes that were differentially expressed after c-Jun inhibition in LPS cell line with and with no Jun amplification. We compared the consequences of c-Jun inhibition in LP6 (genomically c-Jun amplified) and LPS141 (non-amplified) DDLPS cells after Lentivrus modulation. We used lentivirus to deliver 2 control (shGFP, shNT) and 2 Jun (shJun1, shJun3) shRNAs and harvested total RNA on days 4 and 7 after infection, timepoints at which we observed maximum c-Jun inhibition by qRT-PCR and immunoblotting
2014-06-30 | E-GEOD-57529 | biostudies-arrayexpress
Project description:Background: Microorganisms are the major cause of food spoilage during storage, processing and distribution. Pseudomonas fluorescens is a typical spoilage bacterium that contributes to a large extent to the spoilage process of proteinaceous food. RpoS is considered an important global regulator involved in stress survival and virulence in many pathogens. Our previous work revealed that RpoS contributed to the spoilage activities of P. fluorescens by regulating resistance to different stress conditions, extracellular acylated homoserine lactone (AHL) levels, extracellular protease and total volatile basic nitrogen (TVB-N) production. However, RpoS-dependent genes in P. fluorescens remained undefined. Results: RNA-seq transcriptomics analysis combined with quantitative proteomics analysis basing on multiplexed isobaric tandem mass tag (TMT) labeling was performed for the P. fluorescens wild-type strain UK4 and its derivative carrying a rpoS mutation. A total of 375 differentially expressed genes (DEGs) and 212 differentially expressed proteins (DEPs) were identified in these two backgrounds. The DGEs were further verified by qRT-PCR tests, and the genes directly regulated by RpoS were confirmed by 5’-RACE-PCR sequencing. The combining transcriptome and proteome analysis revealed a role of this regulator in several cellular processes, including polysaccharide metabolism, intracellular secretion and extracellular structures, cell well biogenesis, stress responses, ammonia and biogenic amine production, which may contribute to biofilm formation, stress resistance and spoilage activities of P. fluorescens. Moreover, in this work we indeed observed that RpoS contributed to the production of the macrocolony biofilm’s matrix.
2019-11-12 | PXD010845 | Pride
Project description:Elf5 (or ESE-2) is an ETS transcription factor that is abundantly expressed in the mammary epithelium, where it plays a critical role in dictating cell fate and lineage choices. These changes are in part mediated by alterations in the expression and activity of critical components of the Jak/Stat pathway. While the biological function of Elf5 in mammary gland development has been well characterized, its role in breast cancer remains to be elucidated. Here we show that loss of Elf5 leads to features associated with epithelial-mesenchymal transition (EMT) in the mouse mammary gland during pregnancy and lactation. These cellular changes in Elf5-null mammary epithelia are also reflected at the molecular level by the global enrichment of EMT-related gene signatures. ELF5 is expressed in higher level in weakly metastatic breast cancer cells that retained epithelial features compared to highly metastatic cells with mesenchymal features. ELF5 knockdown in T47D breast cancer cells resulted in EMT and increased migration. Conversely, ectopic expression of Elf5 revert mesenchymal-like MDA-MB-231 cells and its lung-tropic variant LM2 to an epithelial phenotype, with reduced migration, invasion and lung metastatic abilities. Finally, we showed that Elf5 binds directly to the promoter of the EMT transcriptional factor Snail2 (Slug) and repress its expression. Taken together, these data established a novel function for Elf5 in inhibiting EMT in normal mammary epithelium and in breast cancer through direct targeting of Snail2. This SuperSeries is composed of the following subset Series: GSE32143: LM2 cell: infected with lentivirus to stably express Elf5 vs GFP GSE32144: MDA-MB-231 cell: infected with lentivirus to stably express mut-Elf5 vs WT-Elf5
2012-09-20 | E-GEOD-32150 | biostudies-arrayexpress
Project description:Many long noncoding transcripts are involved in cancer progression. Here, we utilized high-throughput microarray to compare the transcriptome alterations between the KYSE30 cells overexpressing an empty vector and Epist, thus identified 95 and 99 down-regulated and up-regulated genes, respectively. Expression levels of several previously reported genes implicated in cancer development and progression were altered, such as DDIT3, GATA6, UPP1, FAT3. These genes are involved in tumorigenesis through diverse mechanisms. The present study reveals that Epist functions as a tumor suppressor in Esophageal Squamous Cell Carcinoma. KYSE30 cells overexpressing an empty vector were compared to KYSE30 cells overexpressing Epist. Three biological replicates of each condition were analysed on Agilent microarray.
2015-01-09 | E-GEOD-64792 | biostudies-arrayexpress
Project description:To identify potential biological functions for three lncRNAs (NANCI, LL12, and LL34) we used shRNAs to knockdown expression of lncRNAs in MLE12 cells, a cell resembling type two lung epithelial cells. This data set contains the microarrays looking at gene expression. We used biological triplicate for each shRNA treatment and each treatment group was compared to a biological triplicate of MLE12 cells treated with a scrambled shRNA.
2014-07-22 | E-GEOD-52389 | biostudies-arrayexpress
Project description:The goal of this study was to determine if knockdown of nicastrin induced a proinflammatory phenotype in HEK001 and HEK293 cells. Nicastrin (NCSTN) is a member of the gamma-secretase complex, and has been identified as the most frequently mutated gene in familial hidradenitis suppurativa. While much research has been done into the effects of PSEN1 and PSEN2 loss, less is known about isolated NCSTN haploinsufficiency. Two cell lines were knocked down with either NCSTN siRNA or an siRNA to luciferase in triplicate. RNA was extracted from drug selected knockdowns and profiled on the Illumina Human HT-12 v4 beadarray. Gene ontology analysis of differentially expressed genes revealed a proinflammatory and decreased proliferation signature in keratinocytes. HEK293 cells demonstrated expression signatures for decreased cholesterol synthesis and interferon-alpha signaling, as well as increased p53 signaling and caspase mediated cytoskeletal cleavage. 12 total samples. Two cell lines (HEK001 & HEK293) each with two treatments (NCSTN siRNA knockdown or pLKO luciferase knockdown) in three parallel 3 replicates each. For each line gives the changes specific to knockdown of gamma-secretase component nicastrin (NCSTN).
2014-11-26 | E-GEOD-57949 | biostudies-arrayexpress
Project description:Lentivirus mediated RNAi was used to silence TCEB1 expression in PC-3 prostate cancer cell line. Whole human genome microarray was used to study changes in gene expression induced by the silencing.
2008-10-31 | E-MEXP-1627 | biostudies-arrayexpress
Project description:We aimed to investigate the involvement of genes in the down-regulation of KRT19 in Huh7 cell lines. Stably knocked down KRT-19 in Huh7, the corresponding empty plasmid of PLL3.7 treated control cells were applied to extract the total RNA from three samples in each group, and were amplified and transcribed into fluorescent complementary DNA (cDNA). Labeled samples were hybridized to the Human Roche NimbleGen mRNA microarray (Roche, Basel, Switzerland).
2015-01-19 | E-MTAB-2559 | biostudies-arrayexpress
Project description:In a previous study, we found that H2S alleviates salinity stress in cucumber by maintaining the Na+/K+ balance and by regulating H2S metabolism and the oxidative stress response. However, little is known about the molecular mechanisms behind H2S-regulated salt-stress tolerance in cucumber. Here, an integrated transcriptomic and proteomic analysis based on RNA-seq and 2-DE was used to investigate the global mechanism underlying H2S-regulated salt-stress tolerance. In total, 11 761 differentially expressed genes (DEGs) and 61 differentially expressed proteins (DEPs) were identified. Analysis of the pathways associated with the DEGs showed that salt stress enriched expression of genes in primary and energy metabolism, such as photosynthesis, carbon metabolism and biosynthesis of amino acids. Application of H2S significantly decreased these DEGs but enriched DEGs related to plant-pathogen interaction, sulfur-containing metabolism, cell defense and signal transduction pathways. Notably, changes related to sulfur-containing metabolism and cell defense were also observed through proteome analysis, such as Cysteine synthase 1, Glutathione S-transferase U25-like, Protein disulfide-isomerase and Peroxidase 2. We present the first global analysis of the mechanism underlying H2S regulation of salt-stress tolerance in cucumber through tracking changes in the expression of specific proteins and genes.
2021-09-09 | PXD020642 | Pride