SOX9 overexpression in melanoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Phil Cheng
PROVIDER: E-GEOD-57463 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:SOX9 is generally not expressed in melanomas with a high proliferative capacity but is expressed in melanomas with a high invasive capacity. Here we overexpress full length SOX9 in M010817, a melanoma cell culture with high proliferative capacity but low invasive capacity.
2014-05-09 | GSE57463 | GEO
Project description:Epigenetic dysregulation is a universal feature of cancer that results in altered patterns of gene expression that drive malignancy. Brain tumors exhibit subtype-specific epigenetic alterations, however the molecular mechanisms responsible for these diverse epigenetic states remain unclear. Here we show that the developmental transcription factor Sox9 differentially regulates epigenomic states in high-grade glioma (HGG) and ependymoma (EPN). These contrasting roles for Sox9 correspond with protein interactions with histone deacetylating complexes in HGG, and association with the Rela oncofusion in EPN. Together, our studies demonstrate how epigenomic states are differentially regulated in distinct subtypes of brain tumors, while revealing divergent roles for Sox9 in HGG and EPN tumorigenesis.
2022-07-13 | PXD033863 | Pride
Project description:To identify novel downstream target genes of SOX9, transcriptome analysis of SOX9 transfected human embryonic testicular cell line, NT2/D1, was carried out.
2015-04-30 | E-MTAB-3378 | biostudies-arrayexpress
Project description:Transcriptional profiling of intestinal epithelial cells expressing either Negative, Sublow, Low or High levels of the Sox9-EGFP reporter transgene FACS-isolated from jejunum of non-irradiated mice or at 5 days after 14Gy abdominal irradiation. 4 distinct cell populations, FACS-isolated based on expression levels of the Sox9-EGFP reporter transgene (Sox9-EGFP Negative, Sublow, Low and High cells); 2 conditions: Non-irradiated vs Irradiated; Biological replicates: 7 independent non-irradiated mice and 3 independent irradiated (studied at day 5 post-irradiation) mice
2012-06-17 | E-GEOD-32227 | biostudies-arrayexpress
Project description:Transcriptional profiling of intestinal epithelial cells expressing either Negative, Sublow, Low or High levels of the Sox9-EGFP reporter transgene FACS-isolated from jejunum of non-irradiated mice or at 5 days after 14Gy abdominal irradiation. In both groups, mice were treated for 5 consecutive days with either IGF1 or vehicle via mini-pumps (Alzet 1007D, IGF1 at 10mg/ml) implanted subcutaneously immediately following radiation. 4 distinct cell populations FACS-isolated based on levels of expression of the Sox9-EGFP reporter transgene (Sox9-EGFP Negative, Sublow, Low and High cells). 4 conditions: Non-irradiated/vehicle vs Non-irradiated/IGF1 vs Irradiated/vehicle vs Irradiated/IGF1. Biological replicates: 7 independent non-irradiated mice treated with vehicle - 3 independent non-irradiated mice treated for 5 days with IGF1 - 3 independent irradiated mice studied at day 5 post-irradiation treated with vehicle - 3 independent irradiated mice studied at day 5 post-irradiation treated for 5 days with IGF1.
2015-04-14 | E-GEOD-42817 | biostudies-arrayexpress
Project description:We used two Sertoli-cell-specific Cre lines: Wt1-CreERT2 and Sox9-CreERT2, to induce Sox9 ablation on a Sox8 -/- background in the adult testis. Sox9/8 double KO testes undergo testis-to-ovary genetic reprogramming and Sertoli-to-granulosa cell transdifferentiation.
2016-06-08 | E-MTAB-4572 | biostudies-arrayexpress
Project description:The main goal of our study is to identify the molecular events that determine the gonadal identity in mammals. Although testis and ovary arise from a common embryonic primordium, they represent outcomes of opposing fate determination. This decision to differentiate into a testis or an ovary hinges upon the balance between two antagonizing factors, pro-testis SOX9 and pro-ovary β-catenin. This microarray analysis led to the identification of the genes involved in the fate of XX and XY gonads in absence of SOX9 and beta-catenin We developed mouse genetic models that lack either Sox9, β-catenin, or both specifically in the somatic cells. All embryos used in this study resulted from the crossing between Ctnnb1f/f; Sox9f/f females with Sf1-cre+/Tg ; Ctnnb1+/f; Sox9+/f males. XX and XY fetal gonads were collected at embryonic day E14.5
2015-05-26 | E-GEOD-67463 | biostudies-arrayexpress
Project description:Introduction: In addition to the well-known cartilage extracellular matrix-related expression of Sox9, we demonstrated that chondrogenic differentiation of progenitor cells is driven by a sharply defined bi-phasic expression of Sox9: an immediate early and a late (extracellular matrix associated) phase expression. In this study we aimed to determine what biological processes are driven by Sox9 during this early phase of chondrogenic differentiation. Materials: Sox9 expression in ATDC5 cells was knocked-down by siRNA transfection at the day before chondrogenic differentiation or at day 6 of differentiation. Samples were harvested at 2 hours, and 7 days of differentiation. The mRNA sequencing library was generated using TruSeq mRNA sample preparation kit (Illumina, Eindhoven, the Netherlands). In short, mRNA was enriched using magnetic beads coated with poly-dT, followed by fragmentation. The fragmented mRNA enriched samples were subjected to cDNA synthesis by reverse transcriptase, followed by dA-tailing and ligation of specific double-stranded bar-coded adapters. Next, the library was amplified and following cleanup the sizes of the libraries were determined on an Agilent 2100 Bioanalyzer via a DNA 1000 chip according manufacturer’s protocol. Pooled libraries consisting of equal molar samples were sequenced on a high-output 75bp single read on the NextSeq500 (Illumina). For each sample, the number of reads covering one or more exons of a given transcript were extracted. Triplicates of samples that were treated with either Scrambled or Sox9 siRNAs, at two different time points, were grouped separately. A transcript was defined as expressed when all replicates of a group had at least 5 reads extracted within the transcript's region. The grouped data were then compared to one another. The fold-change difference and the p-value were calculated using R-package edgeR, after which the p-value was corrected for multiple testing (false discovery rate (FDR)-corrected). The transcriptomes using a RNA-seq approach was analyzed using pathway and network analyses. Results: Early Sox9 knockdown severely inhibited chondrogenic differentiation weeks later. Sox9 expression during the immediate early phase of ATDC5 chondrogenic differentiation regulated the expression of ribosome biogenesis factors and ribosomal protein subunits. This was accompanied by decreased translational capacity following Sox9 knockdown, and this correlated to lower amounts of active mono- and polysomes. Moreover, cap- versus IRES-mediated translation was altered by Sox9 knockdown. Sox9 overexpression was able to induce reciprocal effects to the Sox9 knockdown.
2021-06-01 | E-MTAB-10333 | biostudies-arrayexpress
Project description:Extracellular matrix (ECM) deposition and resultant scar play a major role in the pathogenesis and progression of liver fibrosis. Identifying core regulators of ECM deposition may lead to urgently needed diagnostic and therapetic strategies for the disease. The transcription factor Sex determining region Y box 9 (SOX9) is actively involved in scar formation and its prevalence in patients with liver fibrosis predicts progression. In this study, transcriptomic approaches of Sox9-abrogated myofibroblasts identified >30% of genes regulated by SOX9 relate to the ECM.
2019-07-01 | E-MTAB-7298 | biostudies-arrayexpress
Project description:We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly through a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis. Incorportation of ChIP-seq data of Sox9 and histone modification marks for chromatin status together with micorarray gene expression profiling in neonatal mice chondrocytes to uncover Sox9 regulatory system. Overexpression of Sox9 with a control of EGFP in human fibroblasts to identify the direct targets of Sox9 regulatory system
2015-07-01 | E-GEOD-69110 | biostudies-arrayexpress