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Smad3, Smad4 and TTF-1/NKX2-1 binding sites in H441/A549 lung cancer cell lines

ABSTRACT: We evaluated the role of TTF-1/NKX2-1 on Smad3 and Smad4 binding in lung cancer cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51509 | GEO | 2014/07/27

SECONDARY ACCESSION(S): PRJNA223330

REPOSITORIES: GEO

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Smad3, Smad4 and TTF-1/NKX2-1 binding sites in H441/A549 lung cancer cell lines

Project description:We evaluated the role of TTF-1/NKX2-1 on Smad3 and Smad4 binding in lung cancer cell lines. Smad3 binding sites in A549 cells and Smad3, Smad4, and TTF-1/NKX2-1 binding sites in H441 cells were determined by ChIP-seq.

2014-07-27 | E-GEOD-51509 | biostudies-arrayexpress

Expression data of human lung adenocarcinoma cell line H441 treated with TTF-1/NKX2-1 siRNA and TGF-beta

2014-07-27 | GSE49675 | GEO

Expression data of human lung adenocarcinoma cell line H441 treated with TTF-1/NKX2-1 siRNA and TGF-beta

Project description:We determined and analyzed the effect of TTF-1/NKX2-1 on Smad3/Smad4 binding sites by ChIP-sequencing. We used expression microarrays to evaluate the effect of TTF-1/NKX2-1 siRNA on TGF-beta-induced gene expressions. H441 cells were transfected with siRNAs and treated with TGF-beta for RNA extraction and hybridization on Affymetrix microarrays. This submission represents transcriptome component of study.

2014-07-27 | E-GEOD-49675 | biostudies-arrayexpress

TTF-1/NKX2-1 and ASCL1 binding regions in NCI-H209 and NKX2-1 binding regions in NCI-H441, replicate 2

2019-11-30 | GSE139868 | 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

Effect of TTF-1/NKX2-1 expression on TGF-beta induced gene expression in A549 lung cancer cell line.

Project description:TTF-1/NKX2-1 was expressed by adenoviral vector and changes in gene expression were determined by RNA-sequencing. A549 cells were infected with Ad-TTF-1 or Ad-LacZ vectors and stimulated with TGF-beta for 24 hours or left untreated. Expression of polyA RNA was determined.

2014-07-27 | E-GEOD-56356 | biostudies-arrayexpress

Effect of TTF-1/NKX2-1 expression on TGF-beta induced gene expression in A549 lung cancer cell line.

Project description:TTF-1/NKX2-1 was expressed by adenoviral vector and changes in gene expression were determined by RNA-sequencing.

2014-07-27 | GSE56356 | 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

A Smad3 and TTF-1/NKX2-1 complex regulates Smad4-independent gene expression.

Project description:Thyroid transcription factor-1 (TTF-1, also known as NKX2-1) is a tissue-specific transcription factor in lung epithelial cells. Although TTF-1 inhibits the epithelial-to-mesenchymal transition induced by transforming growth factor-β (TGF-β) in lung adenocarcinoma cells, the mechanism through which TTF-1 inhibits the functions of TGF-β is unknown. Here we show that TTF-1 disrupts the nuclear Smad3-Smad4 complex without affecting the nuclear localization of phospho-Smad3. Genome-wide analysis by chromatin immunoprecipitation followed by sequencing revealed that TTF-1 colocalizes with Smad3 on chromatin and alters Smad3-binding patterns throughout the genome, while TTF-1 generally inhibits Smad4 binding to chromatin. Moreover, Smad3 binds to chromatin together with TTF-1, but not with Smad4, at some Smad3-binding regions when TGF-β signaling is absent, and knockdown of Smad4 expression does not attenuate Smad3 binding in these regions. Thus, TTF-1 may compete with Smad4 for interaction with Smad3, and in the presence of TTF-1, Smad3 regulates the transcription of certain genes independently of Smad4. These findings provide a new model of regulation of TGF-β-Smad signaling by TTF-1.

| S-EPMC4123303 | biostudies-literature

Analysis of Nkx2-1-regulated gene expression in A549 lung carcinoma cells

Project description:A transcription factor Nkx2-1 (also known as TTF-1) regulates the expression of different sets of genes. Gene expression analysis was performed using mRNAs from Nkx2-1-induced A549 cells compared to that from the control A549 cells. We used microarrays to detail the global program of gene expression controlled by Nkx2-1 and identified distinct classes of up-regulated and down-regulated genes. mRNAs were isolated from control and Nkx2-1-induced A549 cells and hybridized on Affymetrix microarrays. We sought to identify genes influenced by Nkx2-1.

2012-09-05 | E-GEOD-40584 | biostudies-arrayexpress

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