Evidence map›Paper›PMID 27396952›Full record

ArticleMolecular oncology2016

SNHG16 is regulated by the Wnt pathway in colorectal cancer and affects genes involved in lipid metabolism.

Lise Lotte Christensen, Kirsten True, Mark P Hamilton, Morten M Nielsen, Nkerorema D Damas, Christian K Damgaard, Halit Ongen, Emmanouil Dermitzakis, Jesper B Bramsen, Jakob S Pedersen and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 227 citations in OpenAlex.

  1. Pooled it
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  11. siRNA-based strategies to combat drug resistance in gastric cancer.Medical oncology (Northwood, London, England) · 2024
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  15. The mMolecular cancer · 2024
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48 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

18 authors at 7 institutions in 3 countries.

Lise Lotte ChristensenDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: liselotte.christensen@clin.au.dk.
Kirsten TrueDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: Kirsten_true@hotmail.com.
Mark P HamiltonDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA. Electronic address: mphamilt@bcm.edu.
Morten M NielsenDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: morten.muhlig@clin.au.dk.
Nkerorema D DamasBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark. Electronic address: Nkerorema.Damas@bric.ku.dk.
Christian K DamgaardDepartment of Molecular Biology and Genetics, University of Aarhus, Denmark. Electronic address: ckd@mbg.au.dk.
Halit OngenDepartment of Genetic Medicine and Development, Functional Population Genomics and Genetics of Complex Traits Lab, University of Geneva Medical School, Geneva, Switzerland. Electronic address: Halit.Ongen@unige.ch.
Emmanouil DermitzakisDepartment of Genetic Medicine and Development, Functional Population Genomics and Genetics of Complex Traits Lab, University of Geneva Medical School, Geneva, Switzerland. Electronic address: Emmanouil.Dermitzakis@unige.ch.
Jesper B BramsenDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: bramsen@clin.au.dk.
Jakob S PedersenDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: jakob.skou@clin.au.dk.
Anders H LundBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark. Electronic address: anders.lund@bric.ku.dk.
Søren VangDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: vang@clin.au.dk.
Katrine StriboltDepartment of Pathology, Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: katrine.stribolt@rm.dk.
Mogens R MadsenSurgical Research Unit, Herning Regional Hospital, Herning, Denmark. Electronic address: mogmad@rm.dk.
Søren LaurbergDepartment of Surgery, Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: soerlaur@rm.dk.
Sean E McGuireDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA; Department of Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: Sean.McGuire@bcm.edu.
Torben F ØrntoftDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: orntoft@clin.au.dk.
Claus L AndersenDepartment of Molecular Medicine (MOMA), Aarhus University Hospital, University of Aarhus, Aarhus, Denmark. Electronic address: cla@clin.au.dk.
Aarhus University Hospital · DKUniversity of Copenhagen · DKUniversity of Geneva · CHAarhus University · DKBaylor College of Medicine · USRegionshospitalet Herning · DKThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is well established that lncRNAs are aberrantly expressed in cancer where they have been shown to act as oncogenes or tumor suppressors. RNA profiling of 314 colorectal adenomas/adenocarcinomas and 292 adjacent normal colon mucosa samples using RNA-sequencing demonstrated that the snoRNA host gene 16 (SNHG16) is significantly up-regulated in adenomas and all stages of CRC. SNHG16 expression was positively correlated to the expression of Wnt-regulated transcription factors, including ASCL2, ETS2, and c-Myc. In vitro abrogation of Wnt signaling in CRC cells reduced the expression of SNHG16 indicating that SNHG16 is regulated by the Wnt pathway. Silencing of SNHG16 resulted in reduced viability, increased apoptotic cell death and impaired cell migration. The SNHG16 silencing particularly affected expression of genes involved in lipid metabolism. A connection between SNHG16 and genes involved in lipid metabolism was also observed in clinical tumors. Argonaute CrossLinking and ImmunoPrecipitation (AGO-CLIP) demonstrated that SNHG16 heavily binds AGO and has 27 AGO/miRNA target sites along its length, indicating that SNHG16 may act as a competing endogenous RNA (ceRNA) "sponging" miRNAs off their cognate targets. Most interestingly, half of the miRNA families with high confidence targets on SNHG16 also target the 3'UTR of Stearoyl-CoA Desaturase (SCD). SCD is involved in lipid metabolism and is down-regulated upon SNHG16 silencing. In conclusion, up-regulation of SNHG16 is a frequent event in CRC, likely caused by deregulated Wnt signaling. In vitro analyses demonstrate that SNHG16 may play an oncogenic role in CRC and that it affects genes involved in lipid metabolism, possible through ceRNA related mechanisms.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisCell MovementCell ProliferationCell SurvivalColorectal NeoplasmsCytoplasmGene Knockdown TechniquesHCT116 CellsHumansLipid MetabolismNucleotide MotifsPolyribosomesPromoter Regions, GeneticProto-Oncogene Proteins c-mycRNA, Long NoncodingProto-Oncogene Proteins c-mycRNA, Long NoncodingRNA, Small NucleolarSNHG16 lncRNA, humanTranscription FactorsAGO-CLIPColorectal cancerFunctional analysesLong non-coding RNAsSNHG16Wnt pathway

Identifiers

PMID27396952
PMCPMC5423192
OpenAlexW2465379473

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.