Evidence map›Paper›PMID 24709423›Full record

ArticleNeoplasia (New York, N.Y.)2014

Tumor-suppressive activity of Lunatic Fringe in prostate through differential modulation of Notch receptor activation.

Shubing Zhang, Wen-cheng Chung, Guanming Wu, Sean E Egan, Keli Xu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Decoding the PTM-switchboard of Notch.Biochimica et biophysica acta. Molecular cell research · 2019
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Lunatic, Manic, and Radical Fringe Each Promote T and B Cell Development.Journal of immunology (Baltimore, Md. : 1950) · 2016
    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

5 authors at 3 institutions in 2 countries.

Shubing ZhangCancer Institute, University of Mississippi Medical Center, Jackson, MS.
Wen-cheng ChungCancer Institute, University of Mississippi Medical Center, Jackson, MS.
Guanming WuDepartment of Medical Informatics and Clinical Epidemiology and Oregon Clinical and Translational Research Institute, Oregon Health and Science University, Portland, OR.
Sean E EganProgram in Developmental and Stem Cell Biology, The Hospital for Sick Children and Department of Molecular Genetics, University of Toronto, Toronto, Canada.
Keli XuCancer Institute, University of Mississippi Medical Center, Jackson, MS; Department of Neurobiology and Anatomical Sciences, University of Mississippi Medical Center, Jackson, MS. Electronic address: kxu@umc.edu.
University of Mississippi Medical Center · USOregon Health & Science University · USSickKids Foundation · CA

Funding

Functional analysis of Manic Fringe in the claudin-low breast cancerR21CA175136 · NCI · UNIVERSITY OF MISSISSIPPI MED CTR · PI XU, KELI · 2013 to 2014
$344k
NCI NIH HHS R21 CA175136
6 · The paper itself

Abstract

Elevated Notch ligand and receptor expression has been associated with aggressive forms of prostate cancer, suggesting a role for Notch signaling in regulation of prostate tumor initiation and progression. Here, we report a critical role for Lunatic Fringe (Lfng), which encodes an O-fucosylpeptide 3-ß-N-acetylglucosaminyltransferase known to modify epidermal growth factor repeats of Notch receptor proteins, in regulation of prostate epithelial differentiation and proliferation, as well as in prostate tumor suppression. Deletion of Lfng in mice caused altered Notch activation in the prostate, associated with elevated accumulation of Notch1, Notch2, and Notch4 intracellular domains, decreased levels of the putative Notch3 intracellular fragment, as well as increased expression of Hes1, Hes5, and Hey2. Loss of Lfng resulted in expansion of the basal layer, increased proliferation of both luminal and basal cells, and ultimately, prostatic intraepithelial neoplasia. The Lfng-null prostate showed down-regulation of prostatic tumor suppressor gene NKX3.1 and increased androgen receptor expression. Interestingly, expression of LFNG and NKX3.1 were positively correlated in publically available human prostate cancer data sets. Knockdown of LFNG in DU-145 prostate cancer cells led to expansion of CD44(+)CD24(-) and CD49f(+)CD24(-) stem/progenitor-like cell population associated with enhanced prostatosphere-forming capacity. Taken together, these data revealed a tumor-suppressive role for Lfng in the prostate through differential regulation of Notch signaling.

Indexed as

Genes, Tumor SuppressorAnimalsCell ProliferationGene ExpressionGene Expression Regulation, NeoplasticGlycosyltransferasesHomeodomain ProteinsHumansMaleMice, KnockoutProstateProstatic NeoplasmsProto-Oncogene ProteinsReceptor, Notch1Receptor, Notch2Receptor, Notch3GlycosyltransferasesHomeodomain ProteinsLFNG protein, humanNKX3-1 protein, humanNOTCH1 protein, humanNOTCH2 protein, humanNOTCH3 protein, humanNOTCH4 protein, humanProto-Oncogene ProteinsReceptor, Notch1Receptor, Notch2Receptor, Notch3Receptor, Notch4Receptors, AndrogenReceptors, NotchTranscription Factors

Identifiers

PMID24709423
PMCPMC3978396
OpenAlexW1887565043

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.