ArticleCell death & disease2015
LincRNA-p21 acts as a mediator of ING1b-induced apoptosis.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Microarray analysis of hub genes, non-coding RNAs and pathways in lung after whole body irradiation in a mouse model.International journal of radiation biology · 2023Article
- Biophysical characterisation of human LincRNA-p21 sense and antisense Alu inverted repeats.Nucleic acids research · 2022Article
- Long non-coding RNAs and microRNAs as crucial regulators in cardio-oncology.Cell & bioscience · 2022Review
- ERα determines the chemo-resistant function of mutant p53 involving the switch between lincRNA-p21 and DDB2 expressions.Molecular therapy. Nucleic acids · 2021Article
- HOTAIR beyond repression: In protein degradation, inflammation, DNA damage response, and cell signaling.DNA repair · 2021Review
- Review
- An update on long intergenic noncoding RNA p21: a regulatory molecule with various significant functions in cancer.Cell & bioscience · 2020Review
- Long non-coding RNAs in non-small cell lung cancer: functions and distinctions from other malignancies.Translational cancer research · 2019Review
- Long non-coding RNA NORAD promotes the occurrence and development of non-small cell lung cancer by adsorbing MiR-656-3p.Molecular genetics & genomic medicine · 2019Article
- The anti-tumor activity of brown seaweed oligo-fucoidan via lncRNA expression modulation in HepG2 cells.Cytotechnology · 2019Article
- Induction of a Long Noncoding RNA Transcript, NR_045064, Promotes Defense Gene Transcription and Facilitates Intestinal Epithelial Cell Responses againstJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Co-Administration of Melatonin Effectively Enhances the Therapeutic Effects of Pioglitazone on Mesenchymal Stem Cells Undergoing Indoxyl Sulfate-Induced Senescence through Modulation of Cellular Prion Protein Expression.International journal of molecular sciences · 2018Article
- Critical effects of long non-coding RNA on fibrosis diseases.Experimental & molecular medicine · 2018Review
- TGF-β-induced hepatocyte lincRNA-p21 contributes to liver fibrosis in mice.Scientific reports · 2017Article
- Long noncoding RNAs in the p53 network.Wiley interdisciplinary reviews. RNA · 2017Review
- LincRNa-p21: function and mechanism in cancer.Medical oncology (Northwood, London, England) · 2017Review
- Inverted repeat Alu elements in the human lincRNA-p21 adopt a conserved secondary structure that regulates RNA function.Nucleic acids research · 2016Article
- In Vivo Characterization of Linc-p21 Reveals Functional cis-Regulatory DNA Elements.Cell reports · 2016Article
- LincRNA-p21: Implications in Human Diseases.International journal of molecular sciences · 2015Review
- Defining the minimal peptide sequence of the ING1b tumour suppressor capable of efficiently inducing apoptosis.Cell death discovery · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ING1b is a tumor suppressor that affects transcription, cell cycle control and apoptosis. ING1b is deregulated in disease, and its activity is closely linked to that of p53. In addition to regulating protein-coding genes, we found that ING1b also influences the expression of large intergenic non-coding RNAs (lincRNAs). In particular, lincRNA-p21 was significantly induced after DNA-damage stress or by ING1b overexpression. Furthermore, lincRNA-p21 expression in response to DNA damage was significantly attenuated in cells lacking ING1b. LincRNA-p21 is also a target of p53 and can trigger apoptosis in mouse cell models. We found that this function of lincRNA-p21 is conserved in human cell models. Moreover, ING1b and p53 could function independently to influence lincRNA-p21 expression. However, their effects become more additive under conditions of stress. In particular, ING1b regulates lincRNA-p21 levels by binding to its promoter and is required for induction of lincRNA-p21 by p53. The ability of ING1b to cause apoptosis is also impaired in the absence of lincRNA-p21. Surprisingly, deletion of the ING1b plant homeodomain, which allows it to bind histones and regulate chromatin structure, did not alter regulation of lincRNA-p21. Our findings suggest that ING1b induces lincRNA-p21 expression independently of histone 3 lysine 4 trimethylation mark recognition and that lincRNA-p21 functions downstream of ING1b. Thus, regulation at the level of lincRNA-p21 may represent the point at which ING1b and p53 pathways converge to induce apoptosis under specific stress conditions.
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