Evidence map›Paper›PMID 30323967›Full record

ArticleAmerican journal of cancer research2018

The O-glycosylating enzyme GALNT2 suppresses the malignancy of gastric adenocarcinoma by reducing EGFR activities.

Wan-Ting Hu, Chi-Chuan Yeh, Shin-Yun Liu, Min-Chuan Huang, I-Rue Lai

Abstract read
In one paragraph

Article in American journal of cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Article
  2. GalNAc-Transferases in Cancer.Biomedicines · 2025
    Review
  3. Article
  4. GALNT3 in Ischemia-Reperfusion Injury of the Kidney.Journal of the American Society of Nephrology : JASN · 2025
    Article
  5. Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Protein Glycosylation as Biomarkers in Gynecologic Cancers.Diagnostics (Basel, Switzerland) · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Role of GALNT2 on Insulin Sensitivity, Lipid Metabolism and Fat Homeostasis.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. Observational
  19. Mucin-Type O-GalNAc Glycosylation in Health and Disease.Advances in experimental medicine and biology · 2021
    Article
  20. The Role of APPBiomolecules · 2020
    Review
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.

Wan-Ting HuGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University Taipei, Taiwan.
Chi-Chuan YehDepartment of Surgery, National Taiwan University Hospital Taipei, Taiwan.
Shin-Yun LiuGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University Taipei, Taiwan.
Min-Chuan HuangGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University Taipei, Taiwan.
I-Rue LaiGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant glycosylation affects the malignant progression of cancers. Here, we report that N-acetyl-galactosaminyltransferase 2 (GALNT2), an enzyme that initiates the mucin type-O glycosylation, suppresses malignant phenotypes in gastric adenocarcinoma (GCA) cells by modifying epidermal growth factor receptor (EGFR) activity. GALNT2 was knocked down using siRNA in AGS and MKN28 cells. The expression of phosphorylated EGFR (pEGFR), phosphorylated Akt (pAkt) and Tn antigen were detected by western blotting. Proliferation, migration and invasion of cells with/without GLANT2-knockdown were assessed. Expression of pEGFR in the resected gastric cancer tissue was analyzed by Immunohistochemical staining, and was correlated with clinicopathological factors. The results showed that GALNT2 knockdown enhanced phosphorylation of EGFR and decreased expression of the Tn antigen on EGFR. Inhibiting EGFR activity with Gefitinib decreased the migration/invasion abilities and reversed the increase pAkt caused by GALNT2 knockdown in GCA cells. The addition of MK2206 (Akt inhibitor) mitigated the migration and invasion abilities of the GALNT2-knockdown cells. Patients with increased expressions of pEGFR in their cancer tissues were associated more metastasis, advanced stage and recurrence after surgical resection. Our results indicate that GALNT2 suppresses the malignant potential of GCA cells through the EGFR-Akt signaling pathway. The significance of O-glycosylation in receptor tyrosine kinases activities and GCA progression deserve further studies.

Indexed as

epidermal growth factor receptorgalnac-transferaseGALNT2gastric cancero-glycosylationreceptor tyrosine kinase

Identifiers

PMID30323967
PMCPMC6176175

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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.