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Changes in gene expression caused by RhoH/TTF

ABSTRACT: RhoH/TTF is upregulated in eosinophils by exposure to cytokines. To find out which genes are regulated by RhoH, we investigated changes in gene expression in eosinophilic HL-60c15 cells overexpressing RhoH HL-60c15 transduced with 4-OHT (4-hydroxytamoxifen)-inducible llentiviral constructs coding for RhoH (HL-60-RhoH) were treated or not treated with 4-OHT. 4-OHT-treated HL-60c15 cells transduced with a GFP control construct (HL-60-GFP) were included as an additional controls. Analysis was performed on 3 biological replicates

ORGANISM(S): Homo sapiens

SUBMITTER: Christina Stoeckle

PROVIDER: E-GEOD-64015 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Changes in gene expression caused by RhoH/TTF

Project description:RhoH/TTF is upregulated in eosinophils by exposure to cytokines. To find out which genes are regulated by RhoH, we investigated changes in gene expression in eosinophilic HL-60c15 cells overexpressing RhoH

2014-12-10 | GSE64015 | GEO

mRNA profiles of JMJD3 overexpression- and JMJD3 knockout- HL-60 cells

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of HL-60 cells transduced with control or JMJD3-expression vector, and HL-60 parental and JMJD3 knockout cells

2018-06-13 | GSE100484 | GEO

miRNAs regulated by TTF-1 in small cell lung cancer cell lines

Project description:To determine miRNAs regulated by TTF-1 in SCLC cell lines, miRNA array analyses were carried out in NCI-H209 cells following TTF-1 knockdown

2018-07-10 | GSE106164 | GEO

Gene expression patterns in response to GATA2 (WT and mutants) in HL-60 cells

Project description:GATA2 mutants were discovered in families predisposed to MDS/AML and in sporadic cases of CML-blast crisis. Promyelocytic HL-60 cells were transduced with lentiviral vectors that express GATA2 WT or T354M, 355delT or L359V mutants upon addition of 4-hydroxy tamoxifen (4HT). Microarrays were performed to identify GATA2 WT signatures and differences caused by these mutations. HL-60 cells transduced with GATA2 (WT, T354M, 355delT and L359V) lentiviruses were treated with 4HT for 24 hours and RNA isolated and gene expression measured on Affymetrix microarrays.

2011-08-19 | E-GEOD-29276 | biostudies-arrayexpress

Gene expression profiling of LT-HSCs and ST-HSCs conditionally expressing MLL-ENL

Project description:We have developed a new conditional transgenic mouse showing that MLL-ENL, at an endogenous-like expression level, induces leukemic transformation selectively in LT-HSCs. To investigate the molecular mechanism of leukemic transformation in LT-HSCs conditionally expressing MLL-ENL, we preliminarily performed comprehensive gene expression profiling of CreER-transduced LT-HSCs and ST-HSCs using cDNA microarray analysis. For initial screening of candidate genes invloved in the leukemic transformation, total RNA was extracted from colony-forming cells derived from LT-HSCs and ST-HSCs transduced with CreER or mock. Four samples were analyzed, and CreER-transduced LT/ST-HSC-derived cells were compared with mock-transduced LT/ST-HSC-derived cells, while CreER/mock-transduced LT-HSC-derived cells were compared with CreER/mock-transduced ST-HSC-derived cells.

2013-07-17 | E-GEOD-48539 | biostudies-arrayexpress

Genes regulated by TTF-1 in small cell lung cancer cell lines

Project description:To investigate genes possibly regulated by TTF-1 in small cell lung cancer cell lines, we compared gene expression profiles of NCI-H209 and Lu139 cell lines electroporated with control and TTF-1 siRNAs.

2018-07-11 | GSE106091 | GEO

Overexpression of lung developmental transcription factors TTF-1, NKX2-8 and PAX9

Project description:We investigated the clinical implications of lung developmental transcription factors (TTF-1, NKX2-8, and PAX9) which we recently discovered as cooperating oncogenes activated by way of gene amplification at chromosome 14q13 in lung cancer. Using stable transfectants of human bronchial epithelial cells, RNA expression profiles (signatures) representing activation of the biological pathways defined by each of the three genes were determined and used to risk stratify a non-small cell lung cancer (NSCLC) clinical dataset consisting of ninety-one early stage tumors. Co-activation of the TTF-1 and NKX2-8 pathways identified a cluster of patients with poor survival, representing approximately 20% of patients with early stage NSCLC, whereas activation of individual pathways did not reveal significant prognostic power. Importantly, the poor prognosis associated with co-activation of TTF-1 and NKX2-8 was validated in two other independent clinical datasets. Further, lung cancer cell lines showing co-activation of the TTF-1 and NKX2-8 pathways were shown to exhibit resistance to cisplatin, the standard of care for the treatment of NSCLC. Since TTF-1 and NKX2-8 lack specific inhibitors at the current time, we explored an alternative therapeutic strategy. Using signatures of signaling pathway activation, we identified deregulation of specific oncogenic pathways (Ras and Myc) in the TTF-1/NKX2-8 co-activated cohort. In vitro experiments demonstrated the ability of a Ras pathway-specific therapy to inhibit tumor cell growth in TTF-1/NKX-2 activated cells, thus, suggesting that modulation of the Ras pathway is a rational strategy to targeted therapy in high risk NSCLC patients with co-activation of specific lung developmental pathways. Keywords: Transcription factor expression analysis

2009-04-01 | GSE9212 | GEO

Growth arrest of human thyroid cancer cells 8505C after inhibition of TTF-1 transcriptional activity

Project description:Background: thyroid transcription factor-1 (TTF-1) is known to play key roles in thyroid organogenesis, in thyroid cell proliferation and in the expression of genes involved in thyroid differentiated function. Objective: to understand why many human thyroid cancer cell lines keep producing TTF-1 despite the loss of differentiation. Methods: a chimeric protein acting as a functional antagonist of TTF-1 transcriptional activity was expressed conditionally in 8505C cells originating from an undifferentiated thyroid carcinoma. The consequences of the inhibition of TTF-1 activity in the cells expressing the antagonist on cell proliferation, mRNA and miRNA expression were analyzed. Results: we observed a growth arrest of 8505C thyroid cancer cells when the endogenous TTF-1 transcriptional activity was inhibited. It correlated with decreased levels of several mRNAs encoding positive effectors of cell proliferation like CDK1 and cyclinB1, and increased levels of various mRNAs encoding negative regulators of cell division like CDKN2B and DUSP6. By contrast, no significant change was observed in the miRNA population. Conclusion: the persistence of TTF-1 expression observed in most dedifferentiated human thyroid cancer cell lines is likely to be explained by the fact that TTF-1 activity is still required for proliferation of these tumor cells as demonstrated here in the 8505C cell line.

2016-06-01 | GSE58243 | GEO

Growth arrest of human thyroid cancer cells 8505C after inhibition of TTF-1 transcriptional activity

2015-06-15 | GSE58587 | GEO

RNA-seq transcriptome analysis in NCI-H209 and NCI-H441 cells transfected with TTF-1/NKX2-1 or ASCL1 siRNAs.

Project description:Although Thyroid transcription factor-1 (TTF-1, encoded by NKX2-1 gene) is highly expressed in small cell lung carcinoma (SCLC) and lung adenocarcinoma (LADC), difference in the functional roles of TTF-1 between SCLC and LADC remains to be elucidated. The aim of this study was to clarify the differences in the TTF-1 binding regions and functional roles in SCLC and LADC. Employing chromatin immunoprecipitation-sequencing (ChIP-seq) , here we compared the genome-wide TTF-1-binding profiles and the TTF-1-mediated transcriptional programs in a SCLC and a LADC cell lines. We also investigated ASCL1 binding regions in SCLC cells. To validate whether the changes in TTF-1 or ASCL1 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analyses in H209 cells with TTF-1 or ASCL1 knockdown. Data were also obtained from H441 cells transfected with TTF-1 siRNAs.

2019-11-30 | GSE129340 | GEO

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