Validation of AS1 as novel regulator of tumor resistance to immune cell attack
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA408285 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The experiment was performed to verify wether knockdown of AS1 in combination with TNFa treatment affected the signature of genes involved in tumor cell apoptosis and survival
2020-09-21 | GSE104112 | GEO
Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01). In order to identify novel oncogenic lncRNAs in esophageal adenocarcinogenesis, we carried out RNA-seq of a matched NE-BE-EAC tissue pair
2013-10-21 | E-GEOD-48240 | biostudies-arrayexpress
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified a novel androgen-regulated long non-coding (lnc) RNA, SOCS2-AS1. In order to investigate the SOCS2-AS1 function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines (LNCaP and LTAD) after siSOCS2-AS1 or siSOCS2 treatment. We also treated cells with vehicle or androgen to analyzed the effects of siSOCS2-AS1 on AR function. Observation of androgen dependent gene expression changes after treatmet with siSOCS2-AS1 with microarray.
2016-08-01 | E-GEOD-82224 | biostudies-arrayexpress
Project description:Analysis of tiling array data identified 358 genomic regions commonly enriched by the AS1 and T7 antibody datasets. AS1 antibody data set (AS1 antibody versus mock) and the T7 antibody data set (T7 antibody versus mock)
2013-03-06 | E-GEOD-44872 | biostudies-arrayexpress
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:Our study indicates that lncRNA TRAF3IP2-AS1 serving as a negative regulator of Act1 transcriptional expression and IL-17 signaling pathway activity,recruits SRSF10 to downregulate the transcription of IRF1, which is itself a transcriptional factor for Act1. And the psoriasis-susceptible variant A4165G of TRAF3IP2-AS1 is a gain-of-function mutant that binds more strongly than the wild-type form to SRSF10. It means that TRAF3IP2-AS1 or SRSF10 may be a good target for the treatment of human IL-17-related autoimmune diseases.
2021-01-30 | GSE165781 | GEO
Project description:Characterisation IER3-AS1 interacting proteins using chromatin oligo-affinity precipitation (ChOP) followed by mass spectrometry. The HeLa cell lysates was incubated with biotinylated antisense oligonucleotides (ASO), targeting an experimental target antisense long noncoding RNA IER3-AS1 or a control RNA LacZ. LacZ and IER3-AS1 interacting proteomes were pulldown using Streptavidin beads. The eluted protein samples from both LacZ control ASOs and IER3-AS1 ASOs subjected to mass-spectrometry analyses to identify IER3-AS1 interacting proteins.
2022-10-15 | PXD035704 | Pride
Project description:Epigenetic dysregulation is a common feature of acute myeloid leukemia (AML). Recently it has become clear that long noncoding RNAs (lncRNAs) can play a key role in epigenetic regulation, and consequently also dysregulation. Currently, our understanding of the requirements and roles of lncRNAs in AML is still limited. Using CRISPRi screening, we identified the lncRNA SGOL1-AS1 as an essential regulator of survival in THP-1 AML cells. We use RNA affinity purification using a biotinylated bait to pull down binding partners of the lncRNA, SGOL1-AS1. The identified proteins show a signficant enrichment for chromatin-modifying proteins involved in gene repression and chromosome organization.
2023-06-12 | PXD034329 | Pride
Project description:The aim of this experiment was to assess the on- and off-target effects of MAPT-AS1 expression, and whether mutations/deletions to MAPT-AS1 alter these effects. SHSY5Y cells stably expressing variants of MAPT-AS1 were analyzed by Riboseq and Quantseq.
2021-03-20 | E-MTAB-9921 | biostudies-arrayexpress
Project description:Two wild house mice lines were genetically selected for short and long attack latency. Mice with an attack latency <50s or >600s were considered short attack latency mice (SAL) and long attack latency mice(LAL) respectively. RNA from the hippocampus of 14 SAL or 14 LAL mice was pooled and used as input material for the SAGE libraries. Keywords: other
2003-10-31 | GSE786 | GEO