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Role of TTF-1/NKX2-1, Smad3 and Smad4 on lung cancer cell lines

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

ORGANISM(S): Homo sapiens

SUBMITTER: Isogaya K

PROVIDER: S-ECPF-GEOD-51510 | biostudies-other | 2014 Aug

REPOSITORIES: biostudies-other

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Role of TTF-1/NKX2-1, Smad3 and Smad4 on lung cancer cell lines

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

2014-07-27 | E-GEOD-51510 | biostudies-arrayexpress

Role of TTF-1/NKX2-1, Smad3 and Smad4 on lung cancer cell lines

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-07-27 | GSE51510 | GEO

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

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.

2014-07-27 | GSE51509 | 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.

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Characterizing the developmental pathways TTF-1, NKX2-8, and PAX9 in lung cancer.

Project description:We investigated the clinical implications of lung developmental transcription factors (TTF-1, NKX2-8, and PAX9) that 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 3 genes were determined and used to risk stratify a non-small-cell lung cancer (NSCLC) clinical data set consisting of 91 early stage tumors. Coactivation 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 coactivation of TTF-1 and NKX2-8 was validated in 2 other independent clinical data sets. Furthermore, lung cancer cell lines showing coactivation of the TTF-1 and NKX2-8 pathways were shown to exhibit resistance to cisplatin, the standard of care for the treatment of NSCLC. This suggests that the cohort of patients with coactivation of TTF-1 and NKX2-8 pathways appears to be resistant to standard cisplatin therapy, suggesting the need for alternative therapies in this cohort of high-risk patients.

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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.

| S-ECPF-GEOD-56356 | biostudies-other

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.

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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

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

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