Hepatitis C virus-induced expression profiling of Hepatic and non-hepatic cancer cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Daisuke Okuzaki
PROVIDER: E-GEOD-70781 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:To facilitate accurate measurement of the relative expression levels in Hepatitis C virus infection, we carried out in four human cancer cell lines derived from Hepatic (Hec3B; human hepatoma and Huh7; human hepatocellular carcinoma) or nonhepatic (Hec1B; human endometrial and 293T;human embryonic kidney) cells. These experiments identified several genes , expression of which was altered in the same direction among them with real time PCR analysis. Hepatic (Hec3B and Huh7) or nonhepatic (Hec1B and 293T) cells were examined after HCV infection and after mock-treatment. Each cell line was run in singlet.
2012-05-20 | E-GEOD-32886 | biostudies-arrayexpress
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2013-04-16 | E-GEOD-31457 | biostudies-arrayexpress
Project description:We examined gene expression profiles in the rat whole brains using genome-wide microarray technology, and determined gene expression profiles in 3 rat strains: normotensive WKY, spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). To identify candidate genes involved in the genesis of hypertension in the SHR strains, we compared the gene expression levels at 3 and 6 weeks of age, isolated 407 genes showing a more than 4-fold increase or a less than 1/4-fold decrease. The rat whole brains derived from normotensive WKY, spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP) wereã??examined. Each strain was run in triplicate.
2014-01-24 | E-GEOD-41452 | biostudies-arrayexpress
Project description:We examined gene expression profiles in the rat kidneys using genome-wide microarray technology, and determined gene expression profiles in 3 rat strains: normotensive WKY, spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). To identify candidate genes involved in the genesis of hypertension in the SHR strains, we compared the gene expression levels at 3 and 6 weeks of age, isolated 407 genes showing a more than 4-fold increase or a less than 1/4-fold decrease. The rat kidneys derived from normotensive WKY, spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP) were examined. Each strain was run in triplicate.
2015-07-03 | E-GEOD-41453 | biostudies-arrayexpress
Project description:Lats1 and Lats2 are the mediators of the Hippo pathway that regulates tissue growth and proliferation. Lats1 and Lats2 kinases share 85% sequence identity in the kinase domain. However, their non-kinase regions at the N-terminus are distinct except for Lats conserved domain 1 (LCD1) and LCD2, suggesting that their N-terminal regions are important for Lats1/2-specific functions. In this study, we generated Lats1 knockout mice disrupting the N-terminal region containing LCD1 (Lats1M-NM-^TN/M-NM-^TN). We show that some Lats1M-NM-^TN/M-NM-^TN mice were born safely and grew normally. However, mouse embryonic fibroblasts (MEFs) from Lats1M-NM-^TN/M-NM-^TN mice displayed drastic defects in mitosis, showing enhanced centrosome overduplication, chromosomal misalignment, multipolar spindle formation, chromosome bridging, and cytokinesis failure. Moreover, they displayed accelerated cell cycle and cell growth bypassing a cell-cell contact inhibition like tumor cells, and exhibited anchorage independent growth. Indeed, Lats1M-NM-^TN/M-NM-^TN MEFs produced tumors in nude mice after subcutaneous injection, although the tumor growth rate was much slower than ordinary cancer cells. Furthermore, Yap, the key transcriptional co-activator in the Hippo pathway, was overexpressed and retained stable in Lats1M-NM-^TN/M-NM-^TN MEFs under high cell density, and expression of Lats2 mRNA were down-regulated. Total RNAs were extracted from MEFs under high or low cell density using miRNeasy extraction kit (Qiagen). A Dye-swapped experiment was performed by hybridizing complimentary RNA (cRNA) labeled with either Cyanine (Cy) -3 or Cy-5 (Perkin-Elmer) onto Whole Mouse Genome Oligo Microarray (G4122F; Agilent Technologies). Co-hybridizations were performed and data from Cy3 or Cy5 channels were analyzed as normalized signal intensities rather than as log ratios corresponding to each array.
2012-12-17 | E-GEOD-37871 | biostudies-arrayexpress
Project description:Chromatin modifying activities for construction of appropriate epigenetic landscapes by polycomb repressive complex 2 (PRC2) play an essential role in development and tumorigenesis. However, the spatiotemporal mechanisms by which PRC2 achieves diverse epigenomes for specific tissue or cellular contexts remain poorly understood. Here, we discovered that LATS2 knockout causes dysregulation of PRC2 and subsequent transcriptome changes for differentiation in both mouse and human cells. LATS2 depletion dependent dysregulation of PRC2 also effects H3K4me3 and forms negative feedback loop for maintenance of PRC2. Further analyses reveal that LATS2 on chromatin binds to EZH2 and LATS2 has ability to phosphorylate PRC2 in vitro. These LATS2 dependent H3K27me3 targets are highly induced during neurogenesis, and statistical analysis of glioblastoma multiforme reveals that LATS2-high cases show more dedifferentiated transcriptome and poor prognosis with silencing of H3K27me3 targets. These observations suggest that LATS2-mediated epigenome coordination is pivotal for development and disease, including cancer. The labeled cRNAs from MEFs in two different culture conditions (low density vs high density culture) were subjected to Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F in dye swap setup, resulting in two individual microarrays.
2016-07-26 | E-GEOD-63535 | biostudies-arrayexpress
Project description:For the complete cure of tumors, it is essential to eliminate cancer-initiating cells (CICs). Immunohistochemically, most tumor cells were CD20 and/or CD138 positive in clinical samples of lymphoplasmacytic lymphoma (LPL), and CD20- CD138- cells were hardly detected. Therefore, useful positive markers expressing in a candidate of CICs of LPL are necessary. First, we performed gene expression microarray analysis between CD20- CD138- and CD20+ CD138+ subpopulations using sorted Waldenstrom macroglobulinemia cell line (MWCL-1). Two dye-swap experiment was performed onto Human GE 4Ã44K V2 arrays (G4845A; Agilent Technologies).
2016-02-17 | E-GEOD-73756 | biostudies-arrayexpress
Project description:Chromatin modifying activities for construction of appropriate epigenetic landscapes by polycomb repressive complex 2 (PRC2) play an essential role in development and tumorigenesis. However, the spatiotemporal mechanisms by which PRC2 achieves diverse epigenomes for specific tissue or cellular contexts remain poorly understood. Here, we discovered that LATS2 knockout causes dysregulation of PRC2 and subsequent transcriptome changes for differentiation in both mouse and human cells. LATS2 depletion dependent dysregulation of PRC2 also effects H3K4me3 and forms negative feedback loop for maintenance of PRC2. Further analyses reveal that LATS2 on chromatin binds to EZH2 and LATS2 has ability to phosphorylate PRC2 in vitro. These LATS2 dependent H3K27me3 targets are highly induced during neurogenesis, and statistical analysis of glioblastoma multiforme reveals that LATS2-high cases show more dedifferentiated transcriptome and poor prognosis with silencing of H3K27me3 targets. These observations suggest that LATS2-mediated epigenome coordination is pivotal for development and disease, including cancer. The labeled cRNAs from three pairs of MEFs (Lats2-/- vs Lats2 +/+) from three independent litter were subjected to Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F in dye swap setup, resulting in eight individual microarrays including tehnical replicates.
2016-07-26 | E-GEOD-63536 | biostudies-arrayexpress
Project description:Several innate immune cell subsets have recently been identified to maintain gut homeostasis in both human and mice. Among these subsets, CX3CR1high CD11b+ CD11c+ cells contribute to intestinal tolerance through various mechanisms in mice. However, whether tolerogenic innate myeloid cells are present in the human intestine is not clearly defined. In this manuscript, we identified an intestinal myeloid cell subset possessing tolerogenic ability. HLA-DRhigh CD14+ CD163high cells in the human colon were divided into two subsets based on CD160 expression: CD163high CD160high and CD163high CD160low cells. Both cell subsets exhibited high levels of IL-10 production and high phagocytic activities. CD163high CD160high cells suppressed effector CD4+ T cell proliferation by a Foxp3+ Treg cell induction-independent mechanism. We further observed that the number and suppressive activity of these cells were profoundly decreased in patients with ulcerative colitis (UC). In addition, CD163high CD160high cells in the UC patients showed inflammatory phenotype, such as increased expression of IL6, CD80, and CD86, accompanied with decreased IL10RB expression. Our results highlight that a tolerogenic CD163high CD160high cell subset might be implicated in the prevention of UC development. Gene expression analysis of murine CX3CR1high cells (n=10) and murine blood Ly6c+ CD11b+ monocytes (n=6) were performed using Whole Mouse Genome Microarray Kit, 4x44K V2 (G4846A) as dye-swapped experiments.
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