Evidence map›Paper›PMID 25799278›Full record

ArticlePloS one2015

Lewisy promotes migration of oral cancer cells by glycosylation of epidermal growth factor receptor.

Wei-Ling Lin, Yi-Shiuan Lin, Guey-Yueh Shi, Chuan-Fa Chang, Hua-Lin Wu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Expression of 9-Life (Basel, Switzerland) · 2025
    Article
  2. Glycosylation in Cancer.Handbook of experimental pharmacology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Altered glycosylation in cancer: A promising target for biomarkers and therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Charge and Polarity Preferences forFrontiers in oncology · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Glycoprotein B7-H3 overexpression and aberrant glycosylation in oral cancer and immune response.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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 1 institution in 1 country.

Wei-Ling LinDepartment of Biochemistry and Molecular Biology, National Cheng Kung University, Tainan, Taiwan; Cardiovascular Research Center, National Cheng Kung University, Tainan, Taiwan.
Yi-Shiuan LinDepartment of Biochemistry and Molecular Biology, National Cheng Kung University, Tainan, Taiwan; Cardiovascular Research Center, National Cheng Kung University, Tainan, Taiwan.
Guey-Yueh ShiDepartment of Biochemistry and Molecular Biology, National Cheng Kung University, Tainan, Taiwan; Cardiovascular Research Center, National Cheng Kung University, Tainan, Taiwan.
Chuan-Fa ChangDepartment of Medical Laboratory Science and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Hua-Lin WuDepartment of Biochemistry and Molecular Biology, National Cheng Kung University, Tainan, Taiwan; Cardiovascular Research Center, National Cheng Kung University, Tainan, Taiwan.
National Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant glycosylation changes normal cellular functions and represents a specific hallmark of cancer. Lewisy (Ley) carbohydrate upregulation has been reported in a variety of cancers, including oral squamous cell carcinoma (OSCC). A high level of Ley expression is related to poor prognosis of patients with oral cancer. However, it is unclear how Ley mediates oral cancer progression. In this study, the role of Ley in OSCC was explored. Our data showed that Ley was upregulated in HSC-3 and OC-2 OSCC cell lines. Particularly, glycosylation of epidermal growth factor receptor (EGFR) with Ley was found in OC-2 cells, and this modification was absent upon inhibition of Ley synthesis. The absence of Ley glycosylation of EGFR weakened phosphorylation of AKT and ERK in response to epidermal growth factor (EGF). Additionally, EGF-triggered cell migration was reduced, but cell proliferation was not affected. Ley modification stabilized EGFR upon ligand activation. Conversely, absence of Ley glycosylation accelerated EGFR degradation. In summary, these results indicate that increased expression of Ley in OSCC cells is able to promote cell migration by modifying EGFR which in turn stabilizes EGFR expression and downstream signaling. Targeting Ley on EGFR could have a potential therapeutic effect on oral cancer.

Indexed as

Cell MovementProtein Processing, Post-TranslationalCarcinoma, Squamous CellCell Line, TumorCells, CulturedErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGlycosylationHumansKeratinocytesLewis Blood Group AntigensMaleMouth NeoplasmsProto-Oncogene Proteins c-aktErbB ReceptorsExtracellular Signal-Regulated MAP KinasesLewis Blood Group AntigensLewis Y antigenProto-Oncogene Proteins c-akt

Identifiers

PMID25799278
PMCPMC4370659
OpenAlexW2076202104

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.