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Effect of YAP overexpression on HuCCT1 cholangiocarcinoma cell line transcriptome

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Yann Abraham

PROVIDER: E-GEOD-61767 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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YAP promotes proliferation, chemoresistance, and angiogenesis in human cholangiocarcinoma through TEAD transcription factors.

Marti Patricia P Stein Claudia C Blumer Tanja T Abraham Yann Y Dill Michael T MT Pikiolek Monika M Orsini Vanessa V Jurisic Giorgia G Megel Philippe P Makowska Zuzanna Z Agarinis Claudia C Tornillo Luigi L Bouwmeester Tewis T Ruffner Heinz H Bauer Andreas A Parker Christian N CN Schmelzle Tobias T Terracciano Luigi M LM Heim Markus H MH Tchorz Jan S JS

Hepatology (Baltimore, Md.) 20150825 5

<h4>Unlabelled</h4>The Yes-associated protein (YAP)/Hippo pathway has been implicated in tissue development, regeneration, and tumorigenesis. However, its role in cholangiocarcinoma (CC) is not established. We show that YAP activation is a common feature in CC patient biopsies and human CC cell lines. Using microarray expression profiling of CC cells with overexpressed or down-regulated YAP, we show that YAP regulates genes involved in proliferation, apoptosis, and angiogenesis. YAP activity pro ...[more]

PMID: 26173433

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Effect of YAP overexpression on HuCCT1 cholangiocarcinoma cell line transcriptome (YAPS94A)

Project description:The YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established We used microarrays to assess the role of YAP pathway in cholangiocarcinoma either by overexpressing a constitutively active YAP1 mutant, or by downregulating YAP1 expression using shRNA HuCCT1 cells where transfected with either an empty vector or a vector overexpressing the constitutively active YAP1 S127A; cells were harvested, RNA was collected and analyzed using microarray

2016-06-30 | E-GEOD-69655 | biostudies-arrayexpress

Effect of YAP overexpression on HuCCT1 cholangiocarcinoma cell line transcriptome (YAP overexpression)

2015-10-27 | E-GEOD-61764 | biostudies-arrayexpress

Effect of YAP overexpression on HuCCT1 cholangiocarcinoma cell line transcriptome (shRNA targeting YAP)

Project description:The YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established We used microarrays to assess the role of YAP pathway in cholangiocarcinoma either by overexpressing a constitutively active YAP1 mutant, or by downregulating YAP1 expression using shRNA HuCCT1 cells where transfected with either a control scrambled shRNA or a shRNA targeting YAP1; cells were harvested, RNA was collected and analyzed using microarray

2015-10-27 | E-GEOD-61765 | biostudies-arrayexpress

RISC-mediated control of selected chromatin regulators stabilizes ground state pluripotency of mouse embryonic stem cells (miRNA-Seq)

Project description:We performed an integrated analysis of RNA and proteins at the transition between naÃ¯ve ES cells and cells primed to differentiate. During this transition, mRNAs coding for chromatin regulators were specifically released from translational inhibition mediated by RNA-Induced Silencing Complex (RISC). This suggests that, prior to differentiation, the propensity of ES cells to change their epigenetic status is hampered by RNA interference. The expression of these chromatin regulators was reinstated following acute inactivation of RISC, and it correlated with loss of stemness markers and activation of early cell differentiation markers in treated ES cells. We evaluated global miRNA profiles of embryonic stem cells cultured in either 10%FCS+LIF or 2i+LIF and of Epiblast-Like Aggregates derived from ES cells in 10%FCS+LIF or 2iL+LIF.

2016-03-29 | E-GEOD-79654 | biostudies-arrayexpress

Genome wide analysis of STAT3-mediated transcription and binding sites in mouse female germ stem cell (ChIP-seq)

Project description:Activation of JAK-STAT3 signaling by leukemia inhibitory factor (LIF) is required for maintaining self-renewal of mouse embryonic stem cells (mESCs). STAT3 perform cell type-specific roles in different cell type, here we revisit the role of STAT3 using mouse female germ stem cell (mFGSCs). We applied CRISPR/Cas9 system to generate Stat3 knockout FGSCs and then observed cell growth inhibition and cell cycle arrest in KO cell line. By combining genome wide ChIP-Seq and RNA-Seq, we identified 5990 STAT3 binding sites and discovered serval genes specific regulated by STAT3 that were involved in stem cell proliferation and female gonad development in FGSCs. In general, we identify key roles of STAT3 for sustains self-renewal and proliferation for FGSCs in this study.

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Re-analysis of E-MTAB-1585

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2013-09-19 | E-GEOD-50860 | biostudies-arrayexpress

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2016-02-20 | E-GEOD-75230 | biostudies-arrayexpress

Genome-wide analysis revealed a crosstalk between p53 and the pluripotent gene networks in mouse embryonic stem cells (expression)

Project description:The tumor suppressor p53 regulates the differentiation of embryonic stem (ES) cells upon DNA damage. However, our understanding of this critical tumor suppressive role of p53 in ES cells is limited, mainly because of the lack of molecular mechanism. Here, we report a widespread cross-regulation of p53-mediated DNA damage signaling and the pluripotent gene network in ES cells using chromatin-immunoprecipitation assay-based sequencing (ChIP-seq) and gene expression microarray. Upon DNA damage, p53 directly regulates the transcription of 3644 genes (p<0.005) in mouse ES cells. Genome-wide analysis revealed a dramatic difference between the regulation of p53-activated and -repressed genes. p53 mainly regulates the promoter regions of activated genes, whereas the main regulatory regions for repressed genes reside in distal regions. Among p53-repressed genes, many are pluripotent transcription factors of ES cells, such as Oct4, Nanog, Sox2, Esrrb, c-Myc, n-Myc and Sall4. Strikingly, these transcriptional factors also directly regulate the transcription of the Trp53 gene, highlighting a previously under-estimated transcriptional regulation of p53 in ES cells. Therefore, p53 signaling and ES pluripotent transcriptional networks form an intertwined circuitry. Together, our results provide mechanistic insights into the crosstalk of p53-mediated DNA damage and ES cell "stemness" transcriptional gene networks and shed light on the tumor suppressive function of p53 in ES cells. The goal of this experiment is to identify the gene expression changes after adriamycin treatment in a p53-dependent manner. Total six samples: triplicates for untreated mES cells and triplicates for mES cells treated with adriamycin.

2012-03-05 | E-GEOD-26360 | biostudies-arrayexpress

Expression data of embryonic stem (ES) cells from both control and Prmt6 overexpressed population

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