Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA354395 | ENA |
REPOSITORIES: ENA
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Project description:Ras and its downstream cascades transmit cellular signals, resulting in increased transcription of a large number of genes involved in cell growth and division. Research on long non-coding transcripts regulated by the Ras signaling cascade is still in its infancy. Long non-coding RNAs (lncRNAs) are operationally defined as transcripts that are larger than 200 nt that do not appear to have protein-coding potential. Using a custom-designed lncRNA microarray, we identified a novel lncRNA (oncogenic Ras-induced lncRNA 1, Orilnc1) whose expression is significantly induced by activation of Ras. Further molecular studies demonstrated that the expression of Orilnc1 is regulated by the Ras-Raf-MEK-ERK signaling cascade via the transcriptional factor AP1. Importantly, Orilnc1 is highly expressed in BRAF mutant cancers such as BRAF-driven melanoma. Inhibition of Orilnc1 expression by small RNA interference (siRNA) significantly blocked tumor cell proliferation and growth in vitro and in vivo. Finally, we observed that blocking Orilnc1 reduced expression levels of cell cycle related genes such as Cyclin E1 and induced G1/S arrest in tumor cells. Taken together, Orilnc1 may function as a novel non-protein mediator to respond the Ras/Raf activation and could serve as a potential therapeutic target for RAS or BRAF-driven cancers such as melanoma.
2017-09-05 | GSE90044 | GEO
Project description:Long non-coding RNA landscape in human monocytes
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Project description:The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression [ChIP-Seq]
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Project description:Long non-coding RNAs and mRNAs regulated by TGF-β
| PRJNA237665 | ENA
Project description:Long non-coding RNA expression in Human tissues and cell lines
| PRJNA150189 | ENA
Project description:To identify the the N-Ras-controlled genes in basal-like cells, we used shRNA to repress N-RAS in basal-like SUM102PT, SUM149PT and claudin-low SUM159PT cells. We seek the genes regulated only in basal-like, but not in claudin-low cells, to isolate the genes controlled by N-Ras in a breast cancer subtype-specific fashion. We also overexpressed oncogenic form N-Ras(G12D) in these cells in order to compare the genes regulated by wild-type and oncogenic N-Ras. The shRNA silencing and overexpression were conducted by lentiviral infection in the cells, with non-silencing shRNA-infected cells as the controls. The infected cells were then selected in antibiotics for about 5 days before total RNAs were harvested for microarray analysis. N-Ras was silenced by shRNA or oncogenic N-Ras (G12D) was overexpressed in basal-like SUM102PT, SUM149PT and claudin-low SUM159PT cells.
2015-06-06 | E-GEOD-61768 | biostudies-arrayexpress
Project description:Approximately half of all microRNAs reside within intronic regions and are often co-transcribed with their host genes. However, most studies on intronic microRNAs focus on individual microRNAs, and conversely most studies on protein-coding and non-coding genes frequently ignore any intron-derived microRNAs. We hypothesize that the individual components of such multi-genic loci may play cooperative or competing roles in driving disease progression, and that examining the combinatorial effect of these components would uncover deeper insights into their functional importance. To address this, we perform systematic analyses of intronic microRNA:host loci in colon cancer. We observe that the FTX locus, comprising of a long non-coding RNA FTX and multiple intronic microRNAs, is highly upregulated in cancer and demonstrate that cooperativity within this multi-component locus promotes cancer growth. In addition, we show that FTX interacts with DHX9 and DICER and delineate its novel roles in regulating A-to-I RNA editing and microRNA expression. These results show for the first time that a long non-coding RNA can regulate A-to-I RNA editing, further expanding the functional repertoire of long non-coding RNAs. We further demonstrate the inhibitory effects of intronic miR-374b and -545 on the tumor suppressors PTEN and RIG-I to enhance the proto-oncogenic PI3K-AKT signaling. Finally, we show that intronic miR-421 may exert an autoregulatory effect on miR-374b and -545. Taken together, our data unveil the intricate interplay between intronic microRNAs and their host transcripts in the modulation of key signaling pathways and disease progression, adding new perspectives to the functional landscape of multi-genic loci.
2021-01-05 | PXD021823 | Pride
Project description:Long non-coding RNA expression profiles for 7 human samples derived from patients with laryngeal cancer
| PRJNA255856 | ENA