Evidence map›Paper›PMID 22615920›Full record

ArticlePloS one2012

LGR6 is a high affinity receptor of R-spondins and potentially functions as a tumor suppressor.

Xing Gong, Kendra S Carmon, Qiushi Lin, Anthony Thomas, Jing Yi, Qingyun Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 129 citations in OpenAlex.

  1. Article
  2. Lgr6Genes & diseases · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. R-spondin-1 induces Axin degradation via the LRP6-CK1ε axis.Cell communication and signaling : CCS · 2024
    Article
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  10. Review
  11. Article
  12. Review
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  16. Review
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16 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

6 authors at 2 institutions in 1 country.

Xing GongThe Brown Foundation Institute of Molecular Medicine and Texas Therapeutics Institute, University of Texas Health Science Center at Houston, Houston, Texas, United States of America.
Kendra S Carmon
Qiushi Lin
Anthony Thomas
Jing Yi
Qingyun Liu
The University of Texas Health Science Center at Houston · USBrown Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLGR6 (leucine-rich repeat containing, G protein-coupled receptor 6) is a member of the rhodopsin-like seven transmembrane domain receptor superfamily with the highest homology to LGR4 and LGR5. LGR6 was found as one of the novel genes mutated in colon cancer through total exon sequencing and its promoter region is hypermethylated in 20-50% of colon cancer cases. In the skin, LGR6 marks a population of stem cells that can give rise to all cell lineages. Recently, we and others demonstrated that LGR4 and LGR5 function as receptors of R-spondins to potentiate Wnt/β-catenin signaling. However, the binding affinity and functional response of LGR6 to R-spondins, and the activity of colon cancer mutants of LGR6 have not been determined. PRINCIPAL

findingsWe found that LGR6 also binds and responds to R-spondins 1-3 with high affinity to enhance Wnt/β-catenin signaling through increased LRP6 phosphorylation. Similar to LGR4 and LGR5, LGR6 is not coupled to heterotrimeric G proteins or to β-arrestin following R-spondin stimulation. Functional and expression analysis of three somatic mutations identified in colon cancer samples indicates that one mutant fails to bind and respond to R-spondin (loss-of-function), but the other two have no significant effect on receptor function. Overexpression of wild-type LGR6 in HeLa cells leads to increased cell migration following co-treatment with R-spondin1 and Wnt3a when compared to vector control cells or cells overexpressing the loss-of-function mutant.

conclusionsLGR6 is a high affinity receptor for R-spondins 1-3 and potentially functions as a tumor suppressor despite its positive effect on Wnt/β-catenin signaling.

Indexed as

beta CateninCell MovementColonic NeoplasmsGTP-Binding ProteinsHeLa CellsHumansIntercellular Signaling Peptides and ProteinsMutationProtein BindingReceptors, G-Protein-CoupledSignal TransductionThrombospondinsTumor Suppressor ProteinsWnt Proteinsbeta CateninDKK1 protein, humanGTP-Binding ProteinsIntercellular Signaling Peptides and ProteinsLGR6 protein, humanReceptors, G-Protein-CoupledThrombospondinsTumor Suppressor ProteinsWnt Proteins

Identifiers

PMID22615920
PMCPMC3355120
OpenAlexW2110651281

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.