Global transcriptome profiling was performed for keratinocytes transfected with either miR-146a mimics (Pre-146a) or negative control (Pre-NC).
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE126137 | GEO | 2019/02/07
REPOSITORIES: GEO
Similar Datasets
Project description:Global transcriptome profiling was performed for keratinocytes transfected with either miR-146a mimics (Pre-146a) or negative control (Pre-NC).
| PRJNA521108 | ENA
Project description:Oncogenic mutations in BRAF and NRAS occur in 70% of melanomas. Here we identify a microRNA, miR-146a, that is highly upregulated by oncogenic BRAF and NRAS. Expression of miR-146a increases the ability of human melanoma cells to proliferate in culture and form tumors in mice, whereas knockdown of miR-146a has the opposite effects. We show these oncogenic activities are due to miR-146a targeting the NUMB mRNA, a repressor of Notch signaling. Previous studies have shown that pre-miR-146a contains a single nucleotide polymorphism (C>G rs2910164). We find that the ability of pre-miR-146a/G to activate Notch signaling and promote oncogenesis is substantially higher than that of pre-miR-146a/C. Analysis of melanoma cell lines and matched patient samples indicates that during melanoma progression pre-miR-146a/G is enriched relative to pre-miR-146a/C, resulting from a C-to-G somatic mutation in pre-miR-146a/C. Collectively, our results reveal a central role for miR-146a in the initiation and progression of melanoma.
2014-02-18 | GSE39983 | GEO
Project description:Oncogenic mutations in BRAF and NRAS occur in 70% of melanomas. Here we identify a microRNA, miR-146a, that is highly upregulated by oncogenic BRAF and NRAS. Expression of miR-146a increases the ability of human melanoma cells to proliferate in culture and form tumors in mice, whereas knockdown of miR-146a has the opposite effects. We show these oncogenic activities are due to miR-146a targeting the NUMB mRNA, a repressor of Notch signaling. Previous studies have shown that pre-miR-146a contains a single nucleotide polymorphism (C>G rs2910164). We find that the ability of pre-miR-146a/G to activate Notch signaling and promote oncogenesis is substantially higher than that of pre-miR-146a/C. Analysis of melanoma cell lines and matched patient samples indicates that during melanoma progression pre-miR-146a/G is enriched relative to pre-miR-146a/C, resulting from a C-to-G somatic mutation in pre-miR-146a/C. Collectively, our results reveal a central role for miR-146a in the initiation and progression of melanoma.
2014-02-18 | GSE39294 | GEO
Project description:Oncogenic mutations in BRAF and NRAS occur in 70% of melanomas. Here we identify a microRNA, miR-146a, that is highly upregulated by oncogenic BRAF and NRAS. Expression of miR-146a increases the ability of human melanoma cells to proliferate in culture and form tumors in mice, whereas knockdown of miR-146a has the opposite effects. We show these oncogenic activities are due to miR-146a targeting the NUMB mRNA, a repressor of Notch signaling. Previous studies have shown that pre-miR-146a contains a single nucleotide polymorphism (C>G rs2910164). We find that the ability of pre-miR-146a/G to activate Notch signaling and promote oncogenesis is substantially higher than that of pre-miR-146a/C. Analysis of melanoma cell lines and matched patient samples indicates that during melanoma progression pre-miR-146a/G is enriched relative to pre-miR-146a/C, resulting from a C-to-G somatic mutation in pre-miR-146a/C. Collectively, our results reveal a central role for miR-146a in the initiation and progression of melanoma. SKMEL28 melanoma cell line stably expressing either an empty vector or pre-miR146a with either C or G SNP (SKMEL28-FG12, SKMEL28-miR-146a/C and SKMEL28-miR-146a/G) were used to prepare total RNA. Microarray analysis was performed by using biological replicates for each stable cell lines for a total of 6 samples.
2014-02-18 | E-GEOD-39294 | biostudies-arrayexpress
Project description:5d IL-7-supported bone marrow cultures from C57BL/6 mice deficient for either the transcription factor Bob1 or microRNA-146a Micro-RNAs (miRNAs) are required for many processes during hematopoietic development and activation, including B-cell differentiation. The lymphocyte-specific transcription factor Bob1 is critical for the proper development and function of B cells. Bob1-/- mice are immunodeficient and lack germinal centers. Microarray expression analysis of Bob1-deficient B cells shows numerous up-regulated genes, suggesting that Bob1 may affect targets indirectly via the control of miRNAs. Using a gain-of-function/loss-of-function approach in WEHI-231 and primary pro-B and pre-B cells, we identified miR-146a as a direct target of Bob1. Ttranscriptome-wide analysis of miR-146a-/- B cells shows a number of misregulated genes involved in immune regulation, while analysis of Bob1-/- cells shows increased expression of cell cycle-related genes. These results support previous evidence that Bob1 suppresses proliferation, a previously underappreciated role for Bob1 that is in line with the cancer-prone phenotype of mir-146a-/- mice. 8 samples in total; 2 biological duplicates each of Bob1wt, Bob1KO, wild-type C57BL/6Ncrl, and mir-146aKO
2013-09-07 | E-GEOD-44986 | biostudies-arrayexpress
Project description:5d IL-7-supported bone marrow cultures from C57BL/6 mice deficient for either the transcription factor Bob1 or microRNA-146a Micro-RNAs (miRNAs) are required for many processes during hematopoietic development and activation, including B-cell differentiation. The lymphocyte-specific transcription factor Bob1 is critical for the proper development and function of B cells. Bob1-/- mice are immunodeficient and lack germinal centers. Microarray expression analysis of Bob1-deficient B cells shows numerous up-regulated genes, suggesting that Bob1 may affect targets indirectly via the control of miRNAs. Using a gain-of-function/loss-of-function approach in WEHI-231 and primary pro-B and pre-B cells, we identified miR-146a as a direct target of Bob1. Ttranscriptome-wide analysis of miR-146a-/- B cells shows a number of misregulated genes involved in immune regulation, while analysis of Bob1-/- cells shows increased expression of cell cycle-related genes. These results support previous evidence that Bob1 suppresses proliferation, a previously underappreciated role for Bob1 that is in line with the cancer-prone phenotype of mir-146a-/- mice.
2013-09-07 | GSE44986 | GEO
Project description:Oncogenic mutations in BRAF and NRAS occur in 70% of melanomas. Here we identify a microRNA, miR-146a, that is highly upregulated by oncogenic BRAF and NRAS. Expression of miR-146a increases the ability of human melanoma cells to proliferate in culture and form tumors in mice, whereas knockdown of miR-146a has the opposite effects. We show these oncogenic activities are due to miR-146a targeting the NUMB mRNA, a repressor of Notch signaling. Previous studies have shown that pre-miR-146a contains a single nucleotide polymorphism (C>G rs2910164). We find that the ability of pre-miR-146a/G to activate Notch signaling and promote oncogenesis is substantially higher than that of pre-miR-146a/C. Analysis of melanoma cell lines and matched patient samples indicates that during melanoma progression pre-miR-146a/G is enriched relative to pre-miR-146a/C, resulting from a C-to-G somatic mutation in pre-miR-146a/C. Collectively, our results reveal a central role for miR-146a in the initiation and progression of melanoma. WI-38 cells were either infected with BRAFV600E or Empty retroviral vectors and small RNA were prepared from these cells. As an additional control, WI-38 cells were serum starved and used to generate quiscent cells, which were also used to prepase small RNA. The small RNA were then used to generate small RNA library and were used on Illumina genome analyzer.
2014-02-18 | E-GEOD-39983 | biostudies-arrayexpress
Project description:Human vein umbilical endothelial cells (HUVEC) were transfected with pre-miR control and pre-miR 146 (Ambion) in order to identify targets (direct and indirect) downregulated by miR-146a in endothelial cells. 164 transcripts were downregulated with a fold change ≥ 1.2. Total RNA was obtained from cells transfected in HUVEC with pre-miR control and pre-miR 146a. Three independent transfections were performed for each condition. 2 replicates for control re-control and 3 for pre-miR 146a were analyzed.
2013-12-21 | E-GEOD-43016 | biostudies-arrayexpress
Project description:This study was designed to explore the role of miRNA-146a (miR-146a) and its target genes in the endothelial cells. In this study we have demonstrated that lipopolysaccharide (LPS) induced upregulation of miR-146a in the human umbilical vein endothelial cells (HUVEC) and the induction was blocked by the silencing of the toll-like receptors (TLRs) adaptor molecules MyD88 and nonspecific NF-κB inhibitor BAY 11-7082. In addition, knockdown of miR-146a by transfection of the locked nucleic acid (LNA)-antimiR-146a significantly decreased the increased cell migration and tube formation induced by LPS. A combined analysis of the bioinformatics miRanda algorithms and the whole genome expression microarray of the immunoprecipitated Ago2 ribonucleoprotein complex identified 14 transcripts as the potential target genes. Subsequent transfection with miR-146a precursor pre-miR-146a into the HUVEC validated that the CARD10 was the target gene of the miR-146a both in the transcript and protein level.
2013-09-10 | GSE50619 | GEO
Project description:MiR-146a is an important regulator of innate inflammatory responses and is also implicated in cell death and survival. Here, we identified microglia as the main cellular source of miR-146a among mouse CNS resident cells. We further characterized the phenotype of miR-146a KO microglia cells during in vivo demyelination induced by cuprizone (CPZ) and found reduced number of CD11c+ microglia in the KO compared to WT mice. Microglia were also isolated from the brain, and the proteome was analyzed by liquid chromatography mass spectrometry.
2020-06-29 | PXD015939 | Pride