Evidence map›Paper›PMID 25274627›Full record

ArticleThe Journal of biological chemistry2014

Post-translational glycoprotein modifications regulate colon cancer stem cells and colon adenoma progression in Apc(min/+) mice through altered Wnt receptor signaling.

Huabei Guo, Tamas Nagy, Michael Pierce

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Frizzled receptors: gatekeepers of Wnt signaling in development and disease.Frontiers in cell and developmental biology · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. The Role of Glycosyltransferases in Colorectal Cancer.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Review
  15. Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis.Frontiers in cell and developmental biology · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 2 institutions in 2 countries.

Huabei GuoFrom the Departments of Biochemistry and Molecular Biology, Complex Carbohydrate Research Center and hbguo@uga.edu.
Tamas NagyPathology, College of Veterinary Medicine, University of Georgia, Athens, Georgia 30602.
Michael PierceFrom the Departments of Biochemistry and Molecular Biology, Complex Carbohydrate Research Center and hawkeye@uga.edu.
Carbohydrate Competence Center · NLUniversity of Georgia · US

Funding

TR&D1: Stem Cell and Induced Pluripotent Stem Cell Resources (Pages 116-134)P41GM103490 · NIGMS · UNIVERSITY OF GEORGIA · PI PIERCE, J. MICHAEL · 2012 to 2018
$13.7M
Tumor Glycomics Laboratory for Discovery of Pancreatic Cancer MarkersU01CA128454 · NCI · UNIVERSITY OF GEORGIA · PI PIERCE, J. MICHAEL · 2007 to 2017
$5.7M
NCI NIH HHS U01 CA128454NCI NIH HHS U01CA128454NIGMS NIH HHS P41 GM103490NIGMS NIH HHS P41-GM103490
6 · The paper itself

Abstract

Deletion of GnT-V (MGAT5), which synthesizes N-glycans with β(1,6)-branched glycans, reduced the compartment of cancer stem cells (CSC) in the her-2 mouse model of breast cancer, leading to delay of tumor onset. Because GnT-V levels are also commonly up-regulated in colon cancer, we investigated their regulation of colon CSC and adenoma development. Anchorage-independent cell growth and tumor formation induced by injection of colon tumor cells into NOD/SCID mice were positively associated with GnT-V levels, indicating regulation of proliferation and tumorigenicity. Using Apc(min/+) mice with different GnT-V backgrounds, knock-out of GnT-V had no significant effect on the number of adenoma/mouse, but adenoma size was significantly reduced and accompanied increased survival of Apc(min/+) mice with GnT-V deletion (p < 0.01), suggesting an inhibition in the progression of colon adenoma caused by deletion of GnT-V. Decreased expression levels of GnT-V down-regulated the population of colon (intestine) CSC, affecting their ability for self-renewal and tumorigenicity in NOD/SCID mice. Furthermore, altered nuclear translocation of β-catenin and expression of Wnt target genes were positively associated with expression levels of GnT-V, indicating the regulation of canonical Wnt/β-catenin signaling. By overexpressing the Wnt receptor, FZD-7, in colon cancer cells, we found that FZD-7 receptors expressed N-linked β(1,6) branching, indicating that FZD-7 can be modified by GnT-V. The aberrant Wnt signaling observed after modulating GnT-V levels is likely to result from altered N-linked β(1,6) branching on FZD-7, thereby affecting Wnt signaling, the compartment of CSC, and tumor progression.

Indexed as

Gene Expression Regulation, NeoplasticProtein Processing, Post-TranslationalActive Transport, Cell NucleusAdenomaAdenomatous Polyposis Coli ProteinAnimalsCell Line, TumorCell ProliferationColonic NeoplasmsFemaleGenes, APCGlycoside HydrolasesGlycosylationHumansMiceMice, Inbred C57BLAdenomatous Polyposis Coli Proteinalpha-1,6-mannosylglycoprotein beta 1,6-N-acetylglucosaminyltransferaseGlycoside HydrolasesN-AcetylglucosaminyltransferasesWnt ProteinsApcmin/+ MiceCancer Stem CellsColon CancerGene KnockoutGnT-VN-Linked GlycosylationWnt Signaling

Identifiers

PMID25274627
PMCPMC4223351
OpenAlexW2058222111

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.