Ontology highlight
ABSTRACT:
PROVIDER: PRJNA374924 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identification of splice variants and RNA binding partners of STAT3-induced long noncoding RNAs (STAiRs) in multiple myeloma
| PRJNA376176 | ENA
Project description:Interleukin 6 (IL-6) activates the transcription factor signal transducer and activator of transcription 3 (STAT3). We previously identified several STAT3-induced long noncoding RNAs (STAiRs) in INA-6 multiple myeloma cells (Hackermüller et al. 2014). Here, we analyze five STAiRs by CAPTURE- and ChIRP-RNA-sequencing, a pulldown of a target RNA by transcript tiling oligonucleotides. The CAPTURE technique allows the identification of different STAiR splice variants and shall give rise to the transcript architecture. ChIRP, a method first published by Chu et al 2011, is the original method on which the CAPTURE approach is based on and enables the identification of RNAs interacting with our STAiRs.
2017-08-01 | GSE95131 | GEO
Project description:STAiR18, an mRNA-like STAT3-induced long noncoding RNA shows ubiquitous expression. RNAi-mediated knockdown of STAiR18 led to a dramatic decrease in INA-6 cell vitality. Furthermore, STAiR18 knockdown reduced the STAT3 RNA and protein levels in these cells, suggesting a positive feedback loop between STAT3 and its target ncRNA STAiR18. Microarray analyses of INA-6 cells after STAiR18 or STAT3 knockdown revealed overlapping changes of transcription patterns indicating a close functional interplay between the two molecules. Taken together, STAiR18 represents a novel noncoding RNA that is likely to play an important role for the oncogenic function of the STAT3 pathway. STAT3- and STAiR18-dependent gene expression in human multiple myeloma cell line INA-6 was measured 40 hours after transfection with either a negative control siRNA, an siRNA to STAT3 or an siRNA to STAiR18. Four independent experiments were performed for each siRNA approach, yielding 12 approaches in total.
2016-07-17 | E-GEOD-71092 | biostudies-arrayexpress
Project description:Emerging evidence shows that protein-coding genes can produce noncoding splice forms in addition to their canonical mRNA transcripts. However, the coding-to-noncoding transformation of mRNA and its pathological significance in cancer remain poorly understood. Here, we explored the noncoding variants of protein-coding genes in hepatocellular carcinoma (HCC), and identified a novel sulfotransferase 1C2 (SULT1C2) noncoding variant, lncSULT1C2, as a driver of hepatic tumorigenesis. Polypyrimidine tract-binding protein 1 (PTBP1) mediates the splice switching of SULT1C2 pre-mRNA to lncSULT1C2. Increased lncSULT1C2 expression accelerated the tumorigenicity of HCC cells by reprogramming cholesterol biosynthesis. LncSULT1C2-induced cholesterol accumulation activated mTORC1 signaling and drove the PD-L1-mediated antitumor immune response. High lncSULT1C2 expression decreased the efficacy of anti-PD-1 immunotherapy in mice. GalNAc-conjugated antisense oligonucleotide (ASO) against lncSULT1C2 elicited robust antitumor effects. This study unravels lncSULT1C2 as a previously unrecognized oncogenic noncoding variant of SULT1C2 and highlight the relevance of lncSULT1C2 in cholesterol metabolism reprogramming and tumor immune evasion.
2025-09-23 | PXD068724 |
Project description:Knockdown of STAiR18, an IL-6/STAT3-induced long noncoding RNA, in INA-6 multiple myeloma cells
| PRJNA290335 | ENA
Project description:Detection of RNA–DNA binding sites in long noncoding RNAs
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Project description:RBFOX2 controls the splicing of a large number of transcripts implicated in cell differentiation and development. Parsing RNA-binding protein datasets, we uncover that RBFOX2 can interact with hnRNPC, hnRNPM and SRSF1 to regulate splicing of a broad range of splicing events using different sequence motifs and binding modes. Using immunoprecipitation, specific RBP knockdown, RNA-seq and splice-sensitive PCR, we show that RBFOX2 can target splice sites using three binding configurations: single, multiple or secondary modes. In the single binding mode RBFOX2 is recruited to its target splice sites through a single canonical binding motif, while in the multiple binding mode RBFOX2 binding sites include the adjacent binding of at least one other RNA binding protein partner. Finally, in the secondary binding mode RBFOX2 likely does not bind the RNA directly but is recruited to splice sites lacking its canonical binding motif through the binding of one of its protein partners. These dynamic modes bind distinct sets of transcripts at different positions and distances relative to alternative splice sites explaining the heterogeneity of RBFOX2 targets and splicing outcomes.
2021-06-23 | GSE140679 | GEO
Project description:Long noncoding RNAs (lncRNAs) have appeared to be involved in the most diverse cellular processes through multiple mechanisms. Here we describe a previously uncharacterized human lncRNA, CONCR (cohesion regulator noncoding RNA), transcriptionally activated by MYC, which is upregulated in multiple cancer types. The expression of CONCR is cell cycle-regulated, and it is required for cell cycle progression and DNA replication. Moreover, cells depleted of CONCR show severe defects in sister chromatid cohesion, suggesting an essential role for CONCR in cohesion establishment during cell division. CONCR interacts with and regulates the activity of DDX11, a DNA-dependent ATPase and helicase involved in DNA replication. These findings suggest a novel mechanism of action for CONCR in the modulation of DDX11 enzymatic activity, unveiling the direct involvement of a lncRNA in the establishment of sister chromatid cohesion. Characterization of the function of the long noncoding RNA CONCR. Analysis of DDX11 chromatin binding by ChIP-seq in the presence or absence of CONCR.
2016-08-03 | E-GEOD-81600 | biostudies-arrayexpress
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:A compendium of long non-coding RNAs transcriptional fingerprint in multiple myeloma
| PRJNA430521 | ENA