Evidence map›Paper›PMID 27237318›Full record

ArticleNeoplasia (New York, N.Y.)2016

Morphological Changes, Cadherin Switching, and Growth Suppression in Pancreatic Cancer by GALNT6 Knockdown.

Yunus Emre Tarhan, Taigo Kato, Miran Jang, Yoshimi Haga, Koji Ueda, Yusuke Nakamura, Jae-Hyun Park

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. High-Penetrance Rare Variants Underlying Familial Lung Cancer Risk: Insights From Genetic Epidemiology of Lung Cancer Consortium.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2026
    Article
  3. GalNAc-Transferases in Cancer.Biomedicines · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mucin-Type O-GalNAc Glycosylation in Health and Disease.Advances in experimental medicine and biology · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

7 authors at 2 institutions in 2 countries.

Yunus Emre TarhanDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA.
Taigo KatoDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA.
Miran JangDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA.
Yoshimi HagaCancer Proteomics Group, Genome Center, Japanese Foundation for Cancer Research, Tokyo, 135-8550, Japan.
Koji UedaCancer Proteomics Group, Genome Center, Japanese Foundation for Cancer Research, Tokyo, 135-8550, Japan.
Yusuke NakamuraDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA; Department of Surgery, The University of Chicago, Chicago, IL 60637, USA. Electronic address: ynakamura@bsd.uchicago.edu.
Jae-Hyun ParkDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA.
University of Chicago · USJapanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer reveals the worst prognosis among human cancers with little improvement in its clinical outcome in the last three decades. We previously suggested that polypeptide N-acetylgalactosaminyltransferase 6 (GALNT6), which catalyzes O-type glycosylation of Mucin 1, might be a promising molecular target for drug development for breast cancer. In this study, we report upregulation of GALNT6 in pancreatic cancer cells where Mucin proteins are highly O-glycosylated. We found that knockdown of GALNT6 with small interfering RNA in pancreatic cancer cells decreased the amount of Mucin 4 protein as well as that of its transcript, reduced the levels of human epidermal growth factor receptor 2 and extracellular signal-regulated kinase, and significantly reduced pancreatic cancer cell viability. Interestingly, knockdown of GALNT6 caused drastic morphological changes of pancreatic cells, accompanied with the cadherin switching from P-cadherin to E-cadherin. Considering important roles of Mucin 4 in growth and invasion, our findings imply that targeting GALNT6 is a very promising therapeutic strategy for treatment of pancreatic cancer patients who still have very limited treatment modalities.

Indexed as

CadherinsCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingGlycosylationHumansMucin-4N-AcetylgalactosaminyltransferasesPancreatic NeoplasmsPolypeptide N-acetylgalactosaminyltransferaseRNA, Small InterferingSignal TransductionCadherinsMucin-4N-AcetylgalactosaminyltransferasesPolypeptide N-acetylgalactosaminyltransferaseRNA, Small Interfering

Identifiers

PMID27237318
PMCPMC4887616
OpenAlexW2339917359

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.