ArticleOncogene2013
Cell death/proliferation roles for nc886, a non-coding RNA, in the protein kinase R pathway in cholangiocarcinoma.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 84 citations in OpenAlex.
- Roles of Small Noncoding Vault RNAs in Intestinal Epithelium Homeostasis and Diseases.International journal of molecular sciences · 2025Review
- Toward unraveling molecular grammars for dsRNA-binding proteins: substrate recognition to binding mechanisms.BMB reports · 2025Review
- Vault Particles in Cancer Progression, Multidrug Resistance, and Drug Delivery: Current Insights and Future Applications.International journal of molecular sciences · 2025Review
- Regulation of immunogenic cell death and potential applications in cancer therapy.Frontiers in immunology · 2025Review
- Non-coding 886 (Epigenetics · 2024Review
- The Versatile Roles of nc886, a Fascinating and Peculiar Regulatory Non-Coding RNA, in Cancer.International journal of molecular sciences · 2024Review
- Atypical phosphatase DUSP11 inhibition promotes nc886 expression and potentiates gemcitabine-mediated cell death through NF-kB modulation.Cancer gene therapy · 2024Article
- Human Vault RNAs: Exploring Their Potential Role in Cellular Metabolism.International journal of molecular sciences · 2024Review
- Crosstalk between vault RNAs and innate immunity.Molecular biology reports · 2024Review
- Vault RNAs (vtRNAs): Rediscovered non-coding RNAs with diverse physiological and pathological activities.Genes & diseases · 2024Review
- nc886, an RNA Polymerase III-Transcribed Noncoding RNA Whose Expression Is Dynamic and Regulated by Intriguing Mechanisms.International journal of molecular sciences · 2023Review
- Identification of novel susceptibility methylation loci for pancreatic cancer in a two-phase epigenome-wide association study.Epigenetics · 2022Article
- Adenovirus entry: Stability, uncoating, and nuclear import.Molecular microbiology · 2022Review
- Downregulation ofGenes & diseases · 2022Article
- Small but Powerful: The Human Vault RNAs as Multifaceted Modulators of Pro-Survival Characteristics and Tumorigenesis.Cancers · 2022Review
- Are We Studying Non-Coding RNAs Correctly? Lessons from nc886.International journal of molecular sciences · 2022Review
- A host non-coding RNA, nc886, plays a pro-viral role by promoting virus trafficking to the nucleus.Molecular therapy oncolytics · 2022Article
- Nc886 promotes renal cancer cell drug-resistance by enhancing EMT through Rock2 phosphorylation-mediated β-catenin nuclear translocation.Cell cycle (Georgetown, Tex.) · 2022Article
- Article
- Vault RNAs: hidden gems in RNA and protein regulation.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
We have recently identified nc886 (pre-miR-886 or vtRNA2-1) as a novel type of non-coding RNA that inhibits activation of protein kinase R (PKR). PKR's pro-apoptotic role through eukaryotic initiation factor 2 α (eIF2α) phosphorylation is well established in the host defense against viral infection. Paradoxically, some cancer patients have elevated PKR activity; however, its cause and consequence are not understood. Initially, we evaluated the expression of nc886, PKR and eIF2α in non-malignant cholangiocyte and cholangiocarcinoma (CCA) cells. nc886 is repressed in CCA cells and this repression is the cause of PKR's activation therein. nc886 alone is necessary and sufficient for suppression of PKR via direct physical interaction. Consistently, artificial suppression of nc886 in cholangiocyte cells activates the canonical PKR/eIF2α cell death pathway, suggesting a potential significance of the nc886 suppression and the consequent PKR activation in eliminating pre-malignant cells during tumorigenesis. In comparison, active PKR in CCA cells does not induce phospho-eIF2α nor apoptosis, but promotes the pro-survival nuclear factor-κB pathway. Thus, PKR has a dual life or death role during tumorigenesis. Similarly to the CCA cell lines, nc886 tends to be decreased but PKR tends to be activated in our clinical samples from CCA patients. Collectively from our data, we propose a tumor surveillance model for nc886's role in the PKR pathway during tumorigenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.