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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from human colon cancer cell line HCT116 with NFX1-91 knockdown and control cells

ABSTRACT: NFX1-91, a novel E6 cellular downstream target, functions as a transcriptional regulator and is involved in repressing hTERT expression. Other functions and downstream targets regulated by NFX1-91 were not well understood. We used microarrays to determine gene expression deregulated when NFX1-91 was knocked down. HCT116 cells was infected with lentivirus carrying NFX1-91 shRNA or control β-Galactosidase shRNA to stably knock down target gene expression. Total RNAs were extracted and hybridized on Affymetrix microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Mei Xu

PROVIDER: E-GEOD-23674 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from human colon cancer cell line HCT116 with NFX1-91 knockdown and control cells

Project description:NFX1-91, a novel E6 cellular downstream target, functions as a transcriptional regulator and is involved in repressing hTERT expression. Other functions and downstream targets regulated by NFX1-91 were not well understood. We used microarrays to determine gene expression deregulated when NFX1-91 was knocked down.

2010-08-18 | GSE23674 | GEO

Xanthobacter sp. 91 strain:91

Project description:Xanthobacter sp. 91 strain:91 Genome sequencing and assembly

| PRJNA165239 | ENA

PEA15 regulates the DNA damage induced cell cycle checkpoint and oncogene-directed transformation

Project description:Regulation of the DNA damage response and cell cycle progression is critical for maintaining genome integrity. Here we report that in response to DNA damage, COPS5 deubiquitinates and stabilizes PEA15 in an ATM kinase-dependent manner. PEA15 expression oscillates throughout the cell cycle, and the loss of PEA15 accelerates cell cycle progression by activating CDK6 expression via the c-JUN transcription factor. Cells lacking PEA15 exhibit a DNA damage-induced G2/M checkpoint defect due to increased CDC25C activity and consequentially higher CDK1/Cyclin B activity and accordingly have an increased rate of spontaneous mutagenesis. We find that oncogenic RAS inhibits PEA15 expression and ectopic PEA15 expression blocks RAS-mediated transformation, which can be partially rescued by ectopic expression of CDK6. Finally, we show that PEA15 expression is down regulated in colon, breast and lung cancer samples. Collectively, our results demonstrate that tumor suppressor PEA15 is a regulator of genome integrity and is an integral component of the DNA damage response pathway that regulates cell cycle progression, the DNA-damage-induced G2/M checkpoint and cellular transformation. HCT116 cells stably expressing a non-silencing shRNA or two individual shRNAs against PEA15 were used to prepare the total RNA, which was then used to analyze for gene expression using Illumina expression array.

2014-04-07 | E-GEOD-39297 | biostudies-arrayexpress

Trancriptomic profiling of HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi

Project description:To investigate the influence of PBRM1 on gene expression, we performed RNA-seq in HCT116 colon cancer cells with or without PBRM1 knock-down by RNAi (both shRNA and siRNA approaches were used), and identified differentially expressed genes in PBRM1 knock-down cells compared to control cells, which shows implications for PBRM1's biological function in colon cancer.

2018-01-30 | E-MTAB-5566 | biostudies-arrayexpress

5-hydroxymethylcytosine marks promoters in colon that resist hypermethylation in cancer [Methylation450 Array]

Project description:The discovery of cytosine hydroxymethylation (5-hmC) as a mechanism that potentially controls DNA methylation changes typical of neoplasia prompted us to investigate its behavior in colon cancer. 5-hmC is globally reduced in proliferating cells such as colon tumors and the gut crypt progenitors, from which tumors can arise. Here, we show that colorectal tumors and cancer cells express Ten-Eleven Translocation (TET) transcripts at levels similar to normal tissues. Genome-wide analyses show that promoters marked by 5-hmC in normal tissue, and those identified as TET2 targets in colorectal cancer cells, are resistant to methylation gain in cancer. In vitro studies of TET2 in cancer cells confirm that these promoters are resistant to methylation gain independently of sustained TET2 expression. We also find that a considerable number of the methylation gain-resistant promoters marked by 5-hmC in normal colon overlap with those that are marked with poised bivalent histone modifications in embryonic stem cells. Together our results indicate that promoters that acquire 5-hmC upon normal colon differentiation are innately resistant to neoplastic hypermethylation by mechanisms that do not require high levels of 5-hmC in tumors. Our study highlights the potential of cytosine modifications as biomarkers of cancerous cell proliferation. Six samples were analyzed. 2 biological replicates each of HCT116 cells stably transfected with an empty vector control (TET_KD_Plk), with shRNA to TET2 (TET_KD_2C) and with shRNA to TET2 and TET3 (TET_KD_2.3)

2015-02-03 | E-GEOD-63421 | biostudies-arrayexpress

Escherichia coli strain:C-91 | isolate:C-91

Project description:Escherichia coli strain:C-91 | isolate:C-91 Genome sequencing and assembly

| PRJNA432298 | ENA

Identification of Genes Preferentially Required for Growth of p53-Deficient Human Cancer Cells

Project description:We describe a synthetic interaction screen to identify genes preferentially required for proliferation of p53-deficient human cancer cells. An isogenic pair of p53+/+ and p53-/- human colorectal HCT116 cell lines was stably transduced with a short hairpin RNA (shRNA) library encoded by lentiviruses that integrate in the genomic DNA of the host. Comparison of the frequency of each type of integrated lentivirus in the 2 cell types at an early time point (40hrs) and after about 12 mitotic cycles (10days), reveals genes whose knockdown preferentially impaired growth of p53-/- or p53+/+ HCT116 cells. Keywords: Functional Genomics The region of the integrated lentiviruses is PCR amplified from genomic DNA of the two transduced cell populations at an early and a late time point.

2010-05-01 | E-GEOD-15967 | biostudies-arrayexpress

Psychrobacter celer 91

Project description:Psychrobacter celer 91 genome sequence

| PRJEB270 | ENA

role of miR-146a on Jurkat T cells

Project description:screenning the differentially expressed genes of Jurkat-FF3, Jurkat-miR146a, Jurkat-miR146a-sponge cell lines. To investigate the role of miR-146a on Jurkat T cells, we screened the differentially expressed genes of Jurkat-FF3 (as control), Jurkat-miR146a (as miR-146a overexpression cell line), Jurkat-miR146a-sponge (as miR-146a knock down cell line).

2010-04-03 | E-GEOD-21132 | biostudies-arrayexpress

The histone variant H2A.X is a regulator of EpithelialâMesenchymal Transition

Project description:The epithelial-mesenchymal transition (EMT), considered essential for metastatic cancer, has been a focus of much research, but important questions remain. Here, we show that silencing or removing H2A.X, a histone H2A variant involved in cellular DNA repair and robust growth, induced mesenchymal-like characteristics including activation of EMT transcription factors, Slug and ZEB1, in HCT116 human colon cancer cells. Ectopic H2A.X re-expression partially reversed these changes; as did silencing Slug and ZEB1. In an experimental metastasis model, the HCT116 parental and H2A.X-null cells exhibited similar metastases levels, but the cells with re-expressed H2A.X exhibited substantially elevated levels. We surmise that H2A.X re-expression led to partial EMT reversal and increased robustness in the HCT116 cells, permitting them to both form tumors and to metastasize. In a human adenocarcinoma panel, H2A.X levels correlated inversely with Slug and ZEB1 levels. Together, these results point to H2A.X as a novel regulator of EMT. 9 samples in total including 4 replicates of control shRNA and 5 replicates of shH2A.X.

2016-02-10 | E-GEOD-75444 | biostudies-arrayexpress

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