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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Human gastric cancer cells MKN28 gene expression results: MKN28 cells vs. MKN28 cells with transcription factor Sox2 overexpression

ABSTRACT: Gene expression profiling of gastric cancer cells MKN28 infected with Sox2 lentivirus comparing with MKN28 infected with control lentivirus Transfected cell lines, MKN28-Sox2 vs. MKN28-NC

ORGANISM(S): Homo sapiens

SUBMITTER: Wang Simeng

PROVIDER: E-GEOD-45391 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Human gastric cancer cells MKN28 gene expression results: MKN28 cells vs. MKN28 cells with transcription factor Sox2 overexpression

Project description:Gene expression profiling of gastric cancer cells MKN28 infected with Sox2 lentivirus comparing with MKN28 infected with control lentivirus

2013-05-22 | GSE45391 | GEO

ChIP-DSL H20K promoter array from human gastric cancer cells MKN28 with Sox2 overexpression

Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes. Transcription factor Sox2 promoter array in MKN28 cells with Sox2 overexpression.

2013-05-22 | E-GEOD-45427 | biostudies-arrayexpress

Identification of early targets of SOX2 and PI3K signaling in normal, patient-derived tracheal basal cell lines.

Project description:Microarrays were used to examine gene expression changes in patient derived tracheal basal cell lines after treatment with Lenti-SOX2. Comparisons were made between baseline, Lenti-SOX2 and Lenti-SOX2 with a PI3K inhibitor (BKM120). Total RNA obtained from celll lnes 36 hours post lentivirus addition.

2015-07-01 | E-GEOD-59866 | biostudies-arrayexpress

MKN28 Cells: Vector vs ZIC1 Transfected

Project description:MKN28 cell lines were transfected with pCDNA3.1-ZIC1 or pCDNA3.1 empty vector. Then, an Agilent oligonucleotide microarray was conducted to systematically determine downstream targets of ZIC1.

2012-06-26 | GSE38924 | GEO

Development of a method for quantitative analysis of in vivo interactions of pluripotency transcription factors Sox2, Oct4, Nanog by mass spectrometry

Project description:Protein-protein proximity of core pluripotency transcription factors plays an important role during cell reprogramming. Pluripotent embryonic stem (ES) cell identity is controlled by a trio of transcription factors: Sox2, Oct4, and Nanog. These proteins often bind to closely localized genomic sites. The precise mode by which Sox2, Oct4, and Nanog interact with DNA is likely to make a crucial contribution to their function. Here, a detailed protocol for in vivo detection and quantitative analysis of protein-protein proximity of Sox2 and Oct4 using Proximity Utilizing Biotinylation (PUB) method based on the use of the BAP/BirA (target/enzyme) system is described. The method includes design and cloning of DNA plasmid construct, transient transfection of HEK293T cells, Western blot analysis of nuclei fraction and LC-MS/MS analysis. Experiments with coexpression of BAP-X+BirA-Y (X, Y=Sox2, Oct4 and GFP as control) revealed strong biotinylation level of target proteins when X and Y were pluripotency transcription factors compared with control when X=GFP. Since mass spectrometry provides both high sensitivity and more accurate quantification of data a modified workflow was used, in which SDS-PAGE step was eliminated and His-tagged BAP-fused proteins from cell lysate were purified in 6M guanidine HCl buffer, washed, propionylated, digested directly on the Ni sepharose beads using trypsin and analysed on Q-TOF Impact II instrument. Using mass spectrometry allows making quantitative estimation of in vivo interaction of BAP-Sox2 and BirA-Oct4 which was demonstrated by measuring ratios of biotinylation levels of BAP fused either with Sox2 or GFP at different biotin pulse times. After vector preparation this protocol can be completed in seven working days.

2020-01-21 | PXD015756 | Pride

MKN28 Cells: Vector vs ZIC1 Transfected

2012-06-25 | E-GEOD-38924 | biostudies-arrayexpress

Effect of VPS35 on gene expression in MKN28 gastric cancer cells

Project description:To investigate the function of VPS35 in the regulation of gastric cancer cell proliferation, we established MKN28 cell lines in which VPS35 has been knocked down by shRNA.

2023-05-31 | GSE210320 | GEO

Genome-wide binding of TEAD4 in gastric cancer cell lines MKN28 and SNU216

Project description:To access target binding sites of TEAD4 in gastric cancer, TEAD4 binding was investigated using MKN28 and SNU216 cell lines by ChIP-seq.

2014-01-02 | GSE44416 | GEO

Effect of STAT3c on the gene expression of MKN28 gastric cancer cells

Project description:To investigate the effect of STAT3 activation on the expression of gastric cancer cells, expression profile was compared in MKN28 cells overexpressed with control vector vs mouse constitutively activated STAT3 mutant (STAT3c). MKN28 gastric cancer cells were transfected with pcDNA3.1 (vector control) or plasmid overexpressing STAT3c (treatment). Stable clones were selected for RNA extraction and expression microarray analysis (Agilent). Experiments were repeated twice.

2016-02-27 | E-GEOD-78714 | biostudies-arrayexpress

Competitive binding of E3 ligases TRIM26 and WWP2 controls SOX2 in glioblastoma

Project description:The pluripotency transcription factor SOX2 is essential for the maintenance of glioblastoma stem cells (GSC), which drive tumor growth and treatment resistance.To understand how SOX2 is regulated in GSCs, we utilized a proteomic approach and identified the E3 ubiquitin ligase TRIM26 as a direct SOX2-interacting protein. Unexpectedly, we found TRIM26 depletion decreased SOX2 protein levels and increased SOX2 polyubiquitination in patient-derived GSCs, suggesting TRIM26 promotes SOX2 protein stability. Accordingly, TRIM26 knockdown reduced SOX2 transcriptional activity, self-renewal capacity, and in vivo tumorigenicity in multiple GSC lines. Mechanistically, we found TRIM26, via its C-terminal PRYSPRY domain, but independent of its RING domain, stabilizes SOX2 protein by directly inhibiting the interaction of SOX2 with WWP2, which we identify as a bona fide SOX2 E3 ligase in GSCs. Our work identifies E3 ligase competition as a critical mechanism of SOX2 regulation, with functional consequences for GSC identity and maintenance.

2021-11-04 | PXD028933 | Pride

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