Evidence map›Paper›PMID 26053097›Full record

ArticleOncotarget2015

C/EBPα-p30 protein induces expression of the oncogenic long non-coding RNA UCA1 in acute myeloid leukemia.

James M Hughes, Ivano Legnini, Beatrice Salvatori, Silvia Masciarelli, Marcella Marchioni, Francesco Fazi, Mariangela Morlando, Irene Bozzoni, Alessandro Fatica

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 85 citations in OpenAlex.

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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

James M HughesDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Rome, Italy.
Ivano LegniniDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Rome, Italy.
Beatrice SalvatoriDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Rome, Italy.
Silvia MasciarelliDepartment of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Rome, Italy.
Marcella MarchioniInstitute of Biology, Molecular Medicine and Nanobiotechnology, CNR, Sapienza University of Rome, Rome, Italy.
Francesco FaziDepartment of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Rome, Italy.
Mariangela MorlandoDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Rome, Italy.
Irene BozzoniDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Rome, Italy.
Alessandro FaticaDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Rome, Italy.
Sapienza University of Rome · ITItalian Institute of Technology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidences indicate that different long non-coding RNAs (lncRNAs) might play a relevant role in tumorigenesis, with their expression and function already associated to cancer development and progression. CCAAT/enhancer-binding protein-α (CEBPA) is a critical regulator of myeloid differentiation whose inactivation contributes to the development of acute myeloid leukemia (AML). Mutations in C/EBPα occur in around 10% of AML cases, leading to the expression of a 30-kDa dominant negative isoform (C/EBPα-p30). In this study, we identified the oncogenic urothelial carcinoma associated 1 (UCA1) lncRNA as a novel target of the C/EBPα-p30. We show that wild-type C/EBPα and C/EBPα-p30 isoform can bind the UCA1 promoter but have opposite effects on UCA1 expression. While wild-type C/EBPα represses, C/EBPα-p30 can induce UCA1 transcription. Notably, we also show that UCA1 expression increases in cytogenetically normal AML cases carrying biallelic CEBPA mutations. Furthermore, we demonstrate that UCA1 sustains proliferation of AML cells by repressing the expression of the cell cycle regulator p27kip1. Thus, we identified, for the first time, an oncogenic lncRNA functioning in concert with the dominant negative isoform of C/EBPα in AML.

Indexed as

Gene Expression ProfilingGene Expression Regulation, LeukemicAcute DiseaseBiomarkers, TumorCCAAT-Enhancer-Binding Protein-alphaCell ProliferationCyclin-Dependent Kinase Inhibitor p27HumansImmunoblottingK562 CellsLeukemia, MyeloidMutationPromoter Regions, GeneticProtein BindingProtein IsoformsReverse Transcriptase Polymerase Chain ReactionBiomarkers, TumorCCAAT-Enhancer-Binding Protein-alphaCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p27Protein IsoformsRNA, Long NoncodingUCA1 RNA, humanacute myeloid leukemiaCEBPAlong non-coding RNAUCA1

Identifiers

PMID26053097
PMCPMC4621908
OpenAlexW1853841955

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Registered trials

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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.