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Expression data of NCI-H441 cells stably expressing hsa-mir-365-2 vs empty vector

ABSTRACT: Hsa-mir-365-2 is one of the two precursors that give rise to miR-365. We discovered that miR-365 directly regulates a lung cancer and developmental gene termed thyroid transcription factor 1 (TTF-1 or NKX2-1). Hsa-mir-365-2 was transfected into NCI-H441 cells via retrovirus-mediated gene transfer. Arrays hybridized: Affymetrix GeneChip Human Gene 1.0 ST Array.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33672 | GEO | 2011/11/15

SECONDARY ACCESSION(S): PRJNA148717

REPOSITORIES: GEO

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Expression data of NCI-H441 cells stably expressing hsa-mir-365-2 vs empty vector

Project description:Hsa-mir-365-2 is one of the two precursors that give rise to miR-365. We discovered that miR-365 directly regulates a lung cancer and developmental gene termed thyroid transcription factor 1 (TTF-1 or NKX2-1). Hsa-mir-365-2 was transfected into NCI-H441 cells via retrovirus-mediated gene transfer. Arrays hybridized: Affymetrix GeneChip Human Gene 1.0 ST Array. A total of 4 samples were analyzed. The first two were H441 cells expressing hsa-mir-365-2 and the other two were H441 transfected with empty vector. The class comparison function (significant cutoff, 0.001) of BRB Array Tool (4.1.0 beta_3 release) was used to analyze for differentially expressed genes as a result of enforced expression of hsa-mir-365-2.

2011-11-15 | E-GEOD-33672 | biostudies-arrayexpress

Expression data of NCI-H441 cells stably expressing hsa-mir-365-2 vs empty vector

Project description: Not available

| S-ECPF-GEOD-33672 | biostudies-other

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

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

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 in healthy and SQT1 hiPSC-CMs upon manipulation of miR-365

Project description:Abnormalities of ventricular action potential (AP) cause malignant cardiac arrhythmias and sudden cardiac death. Here, we sought to identify microRNAs (miRNAs) that regulate the human cardiac AP and asked whether their manipulation allows for therapeutic modulation of AP abnormalities. Quantitative analysis of the miRNA targetomes in human cardiac myocytes identified miR-365 as a primary miRNA to regulate repolarizing ion channels. AP recordings in patient-specific induced pluripotent stem cell-derived cardiac myocytes (iPSC-CMs) showed that elevation of miR-365 level significantly prolonged AP duration in hiPSC-CMs derived from a Short-QT syndrome (SQTS) patient, whereas specific inhibition of miR-365 normalized pathologically prolonged AP in Long-QT syndrome (LQTS) iPSC-CMs. Transcriptome analyses in human iPSC-CMs at bulk and single-cell level corroborated the key cardiac repolarizing channels as direct targets of miR-365, together with functionally synergistic regulation of additional AP-regulating genes by this miRNA. Whole-cell patch clamp experiments revealed miR-365-based regulation of repolarizing ionic currents. Finally, refractory period measurements in human myocardial slices substantiated the prolonging effect of miR-365 on AP duration also in adult human myocardial tissue. Our results delineate miR-365 to regulate human cardiac AP duration by targeting key factors of cardiac repolarization.

2021-12-01 | GSE185687 | GEO

single cell RNA-seq in healthy and LQT1 hiPSC-CMs upon manipulation of miR-365

2021-12-01 | GSE185688 | GEO

hsa-miR-503, hsa-miR-103, and hsa-miR-494 genome wide target profiles [RNA-Seq and RIP-Seq]

Project description:We constructed a genome wide target profile of hsa-miR-503, hsa-miR-103, and hsa-miR-494 by sequencing RNA isolated from Ago2 immunoprecipitations and total RNA samples following transfection of the respective miRNA in mature duplex form

2015-02-04 | GSE64615 | GEO

Hsa-miR-371a-5p and hsa-miR-518a-3p regulated genes in choriocarcinoma cells

Project description:We report the application of transcriptome sequencing for investigating of the hsa-miR-371a-5p and hsa-miR-518a-3p regulated genes. JAR, JEG-3 and BeWo choriocarcinoma cells were transfected with hsa-miR-371a-5p or hsa-miR-518a-3p inhibitors or control inhibitors. Totally, 237, 132 and 277 genes with > 2 folds change and adjusted P < 0.05 were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-371a-5p knockdown. Meanwhile, 229, 269 and 191 genes were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-518a-3p knockdown. The top upregulated genes included many oncogenes or oncogenesis associated ones. Enrichment analysis showed hsa-miR-371a-5p and hsa-miR-518a-3p regulated diverse pathways related to tumorigenesis and metastasis. Our results would be helpful for the searching of early molecular biomarkers and therapeutic targets for gestational trophoblastic neoplasia.

2018-11-01 | GSE106394 | GEO

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