KIMAT1 and HIF1A-As2 silencing RNA-seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA512871 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In our study, we valided the important oncogeneic roles of KIMAT1 and HIF1A-As2 in non-small cell lung cancer. We used custom designed GapmeRs to silence the KIMAT1 and HIF1A-As2 in H1299 and performed RNA-seq. 11389 and 7767 genes were regulated by KIMAT1 and HIF1A-As2, respectively.
2020-12-17 | GSE124628 | GEO
Project description:In our study, we valided the important oncogeneic roles of KIMAT1 and HIF1A-As2 in non-small cell lung cancer. We used custom designed GapmeRs to silence the KIMAT1 and HIF1A-As2 in H1299 and performed small RNA-seq. 214 and 233 microRNAs were regulated by KIMAT1 and HIF1A-As2, respectively.
2020-12-17 | GSE124629 | GEO
Project description:KIMAT1 and HIF1A-As2 silencing small RNA-seq
| PRJNA512872 | ENA
Project description:In our study, we valided DHX9 and NPM1 interact with KIMAT1, whereas DHX9 also interacts with HIF1A-As2. DHX9 is a highly conserved DEAD-box protein expressed in the nucleus and the cytoplasm, involved in many processes including transcriptional activation, miRNA biogenesis and tumor cell maintenance. NPM1 is predominantly localized in the nucleoplasm, where it associates with active RNA polymerase II and transcriptionally activates genes involved in cancer. We silenced DHX9 and NPM1 and performed RNA-seq to examine the dysregulated genes by DHX9 and NPM1.
2020-12-17 | GSE124626 | GEO
Project description:In the current study, on the basis of establishment of PA-induced damage model of HUVECs, the silencing and overexpression (OE) of HIF1A-AS1 were implemented in the HUVECs, and the effects on cell viability, apoptosis, migration and invasion were explored, respectively. Functionally, the results indicated silencing of HIF1A-AS1 promoted the proliferation migration and invasion, and reduced the apoptosis of HUVECs. In contrast, OE of HIF1A-AS1 reduced proliferation transwell and invasion, promoted the apoptosis, suggesting that HIF1A-AS1 play vital roles in regulating HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing (RNA-seq) were carried out, and the results indicated that HIF1A-AS1 globally mediate expression of miRNA and mRNA. The multiple target genes of DEmiRNA were associated with cell proliferation and apoptosis, and overlapped with the DEGs from RNA-seq, suggestion that HIF1A-AS1 might regulate the proliferation and apoptosis of HUVECs by regulating miRNA expression.
2024-06-17 | GSE178401 | GEO
Project description:AS1 and AS2 encode MYB related protein and AS2-domain containing protein, respectively and may regulate transcription. These genes are involved in the determination of axes of leaves of Arabidopsis thaliana. To know the gene regulation in the leaf development, expression profile among wild-type, as1 and as2 mutants and AS2 overexpression plants were compaired. shoot apices from as1-1, as2-1, AS2 overexpressing, and wild type embryos
2013-03-01 | E-GEOD-44028 | biostudies-arrayexpress
Project description:In the current study, on the basis of establishment of PA-induced damage model of HUVECs, the silencing and overexpression (OE) of HIF1A-AS1 were implemented in the HUVECs, and the effects on cell viability, apoptosis, migration and invasion were explored, respectively. Functionally, the results indicated silencing of HIF1A-AS1 promoted the proliferation migration and invasion, and reduced the apoptosis of HUVECs. In contrast, OE of HIF1A-AS1 reduced proliferation transwell and invasion, promoted the apoptosis, suggesting that HIF1A-AS1 play vital roles in regulating HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing (RNA-seq) were carried out, and the results indicated that HIF1A-AS1 globally mediate expression of miRNA and mRNA. The multiple target genes of DEmiRNA were associated with cell proliferation and apoptosis, and overlapped with the DEGs from RNA-seq, suggestion that HIF1A-AS1 might regulate the proliferation and apoptosis of HUVECs by regulating miRNA expression.
2024-06-17 | GSE178397 | GEO
Project description:Purpose: to identify genes aberrantly expressed upon myocardial ablation of Hif1a Methods: a floxed Hif1a allele was deleted in mouse embryonic hearts using a NXK2.5Cre line. Total RNA was extracted from E12.5 hearts (n=3 for controls and mutants) usinz Trizol and processed for RNA-seq. Reads were mapped to Mm10 reference genome using TopHat2 and Bowtie2. Transcript expression values were determined after transcript normalization with AltAnalyze Results: this analysis revealed a total of 1451 genes significantely (|Fold| > 20% and P<0.05) modulated in Hif1a cKO hearts 6 total RNAseq runs with 3 experimental samples and 3 controls samples
2015-04-29 | E-GEOD-61209 | biostudies-arrayexpress
Project description:Glioblastoma multiform account for about half of all gliomas and are the most deadly and aggressive forms. Its therapeutic resistance and tumor relapse rely on a subpopulation of cells, the so-called Glioma-stem Cells (GSCs). Here, we investigated for the role of the long non-coding RNA HOXA-AS2 in GSC biology by conducting descriptive and functional analyses of glioma samples classified according to their isocitrate dehydrogenase (IDH1) gene mutation status, and of glioma stem cells. We found that HOXA-AS2 is overexpressed only in aggressive (IDHwt) glioma and GSC. Sh-RNA-based depletion of HOXA-AS2 affects GSC both at the cellular and molecular levels with a decrease in proliferation and altered expression of several hundreds of their genes. Integrative analysis revealed that these changes is expression are not associated to changes in DNA methylation or chromatin signature at the promoter of most deregulated genes following HOXA-AS2 silencing in GSC, supporting a post-transcriptional regulation. In addition, transcription factor motif enrichment and correlation analyses sustained that HOXA-AS2 affect, directly or indirectly, expression of key transcription factors of GCS biology, including E2F8, E2F1, STAT1 and ATF3 to, in fine, contributes to their pathological status by promoting proliferation and modulating the inflammation pathway of Glioma Stem Cell.
2022-04-15 | GSE199031 | GEO
Project description:Glioblastoma multiform account for about half of all gliomas and are the most deadly and aggressive forms. Its therapeutic resistance and tumor relapse rely on a subpopulation of cells, the so-called Glioma-stem Cells (GSCs). Here, we investigated for the role of the long non-coding RNA HOXA-AS2 in GSC biology by conducting descriptive and functional analyses of glioma samples classified according to their isocitrate dehydrogenase (IDH1) gene mutation status, and of glioma stem cells. We found that HOXA-AS2 is overexpressed only in aggressive (IDHwt) glioma and GSC. Sh-RNA-based depletion of HOXA-AS2 affects GSC both at the cellular and molecular levels with a decrease in proliferation and altered expression of several hundreds of their genes. Integrative analysis revealed that these changes is expression are not associated to changes in DNA methylation or chromatin signature at the promoter of most deregulated genes following HOXA-AS2 silencing in GSC, supporting a post-transcriptional regulation. In addition, transcription factor motif enrichment and correlation analyses sustained that HOXA-AS2 affect, directly or indirectly, expression of key transcription factors of GCS biology, including E2F8, E2F1, STAT1 and ATF3 to, in fine, contributes to their pathological status by promoting proliferation and modulating the inflammation pathway of Glioma Stem Cell.
2022-04-15 | GSE199030 | GEO