Evidence map›Paper›PMID 26868975›Full record

ArticleScientific reports2016

Regulation of functional KCNQ1OT1 lncRNA by β-catenin.

Naohiro Sunamura, Takahito Ohira, Miki Kataoka, Daigo Inaoka, Hideyuki Tanabe, Yuji Nakayama, Mitsuo Oshimura, Hiroyuki Kugoh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 74 citations in OpenAlex.

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  10. Long Non-Coding RNAInternational journal of molecular sciences · 2022
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  11. Epigenetic regulation of gastrointestinal cancers mediated by long non-coding RNAs.Cancer biomarkers : section A of Disease markers · 2022
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  13. Oncology research · 2021
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  17. Aging · 2020
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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

8 authors at 2 institutions in 1 country.

Naohiro SunamuraDepartment of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Science, Tottori University, 86 Nishi-Cho, Yonago, Tottori 683-8503, Japan.
Takahito OhiraDepartment of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Science, Tottori University, 86 Nishi-Cho, Yonago, Tottori 683-8503, Japan.
Miki KataokaDepartment of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Science, Tottori University, 86 Nishi-Cho, Yonago, Tottori 683-8503, Japan.
Daigo InaokaDepartment of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Science, Tottori University, 86 Nishi-Cho, Yonago, Tottori 683-8503, Japan.
Hideyuki TanabeDepartment of Evolutionary Studies of Biosystems Science, School of Advanced Sciences, SOKENDAI (The Graduate University for Advanced Studies), Shonan Village, Hayama, Kanagawa 240-0193, Japan.
Yuji NakayamaDivision of Functional Genomics, Research Center for Bioscience and Technology, Tottori University, 86 Nishi-Cho, Yonago, Tottori 683-8503, Japan.
Mitsuo OshimuraChromosome Engineering Research Center, Tottori University, 86 Nishi-Cho, Yonago, Tottori 683-8503, Japan.
Hiroyuki KugohDepartment of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Science, Tottori University, 86 Nishi-Cho, Yonago, Tottori 683-8503, Japan.
Tottori University · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) have been implicated in many biological processes through epigenetic mechanisms. We previously reported that KCNQ1OT1, an imprinted antisense lncRNA in the human KCNQ1 locus on chromosome 11p15.5, is involved in cis-limited silencing within an imprinted KCNQ1 cluster. Furthermore, aberration of KCNQ1OT1 transcription was observed with a high frequency in colorectal cancers. However, the molecular mechanism of the transcriptional regulation and the functional role of KCNQ1OT1 in colorectal cancer remain unclear. Here, we show that the KCNQ1OT1 transcriptional level was significantly increased in human colorectal cancer cells in which β-catenin was excessively accumulated in the nucleus. Additionally, overexpression of β-catenin resulted in an increase in KCNQ1OT1 lncRNA-coated territory. On the other hand, knockdown of β-catenin resulted in significant decrease of KCNQ1OT1 lncRNA-coated territory and an increase in the mRNA expression of the SLC22A18 and PHLDA2 genes that are regulated by KCNQ1OT1. We showed that β-catenin can promote KCNQ1OT1 transcription through direct binding to the KCNQ1OT1 promoter. Our evidence indicates that β-catenin signaling may contribute to development of colorectal cancer by functioning as a novel lncRNA regulatory factor via direct targeting of KCNQ1OT1.

Indexed as

Gene Expression Regulation, Neoplasticbeta CateninCell Line, TumorCell NucleusColorectal NeoplasmsDown-RegulationHEK293 CellsHumansNuclear ProteinsOrganic Cation Transport ProteinsPotassium Channels, Voltage-GatedPromoter Regions, GeneticProtein BindingRNA, Long NoncodingTranscription, Geneticbeta CateninKCNQ1OT1 long non-coding RNA, humanNuclear ProteinsOrganic Cation Transport ProteinsPotassium Channels, Voltage-GatedRNA, Long NoncodingSLC22A18 protein, humanTSSC3 protein

Identifiers

PMID26868975
PMCPMC4751614
OpenAlexW2416077975

What OpenQuestion holds

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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.