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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.

| S-EPMC4123303 | biostudies-literature

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.

| S-EPMC2664027 | biostudies-literature

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

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

Dysregulation of transcripts SMAD4-209 and SMAD4-213 and their respective promoters in colon cancer cell lines.

Project description:Background: The pervasive role of alternative promoters in context-specific isoform expression and the importance of promoter choice over its level of transcriptional activity have been recently implied based on pan-cancer in silico studies. We aimed to explore this phenomenon at the cellular level on the example of a major tumor suppressor SMAD4 in search of molecular mechanisms in colorectal cancer that could be exploited for novel biomarkers or therapeutic approaches. Methods: Multi-omics technologies, in silico tools and in vitro functional assays were applied to analyze the transcripts expression and the alternative promoters' function of the SMAD4 gene in colon cell lines HCEC-1CT, HCT116, DLD-1, SW480 and SW620. Results: High expression of the transcript SMAD4-213 emerged as a hallmark of colon cancer cells, while in silico tools point to its possible additional role and potential for sponging miRNAs. Based on the observed dysregulation of SMAD4-209 and SMAD4-213 in malignant vs. non-malignant colon cells, we propose that their expression ratio might be a solid biomarker candidate for colorectal cancer detection. Conclusions: A differential pattern of the respective promoters' activity was observed that corresponds to the expression of transcripts, confirming the role of alternative promoters in context-specific isoform expression. The investigated SMAD4 promoters and transcripts harbor translational potential that should be further investigated.

| S-EPMC11310865 | biostudies-literature

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