Evidence map›Paper›PMID 29993037›Full record

ArticleOncogene2018

Silencing of MUC20 suppresses the malignant character of pancreatic ductal adenocarcinoma cells through inhibition of the HGF/MET pathway.

Syue-Ting Chen, Ting-Chun Kuo, Ying-Yu Liao, Mei-Chun Lin, Yu-Wen Tien, Min-Chuan Huang

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  11. Article
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  13. Protein Glycosylation as Biomarkers in Gynecologic Cancers.Diagnostics (Basel, Switzerland) · 2022
    Review
  14. Altered glycosylation in pancreatic cancer and beyond.The Journal of experimental medicine · 2022
    Review
  15. Intracellular MUC20 variant 2 maintains mitochondrial calcium homeostasis and enhances drug resistance in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022
    Article
  16. Review
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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

6 authors at 2 institutions in 1 country.

Syue-Ting ChenGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ting-Chun KuoDepartment of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
Ying-Yu LiaoGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Mei-Chun LinDepartment of Otolaryngology, National Taiwan University Hospital, Hsinchu, Hsinchu, Taiwan.
Yu-Wen TienDepartment of Surgery, National Taiwan University Hospital, Taipei, Taiwan. ywtien5106@ntu.edu.tw.
Min-Chuan HuangGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan. mchuang@ntu.edu.tw.
National Taiwan University · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mucins are heavily glycosylated proteins that play critical roles in the pathogenesis of tumour malignancies. Pancreatic ductal adenocarcinoma (PDAC) is characterised by the aberrant expression of mucins. However, the role of mucin (MUC) 20 in PDAC remains unclear. PDAC is usually surrounded by a dense fibrotic stroma consisting of an extracellular matrix and pancreatic stellate cells (PSCs). The stroma creates a nutrient-deprived, hypoxic, and acidic microenvironment, and promotes the malignant behaviours of PDAC cells. In this study, immunohistochemical staining demonstrated that high MUC20 expression correlated with poor progression-free survival and high local recurrence rate of PDAC patients (n = 61). The expression of MUC20 was induced by serum deprivation, hypoxia, and acidic pH in PDAC cells. MUC20 knockdown with siRNA decreased cell viability, as well as migration and invasion induced by PSCs in HPAC and HPAF-II cells. In intraperitoneal, subcutaneous, and orthotopic injection models, MUC20 knockdown decreased tumour growth in immunodeficient mice. Phospho-RTK array and western blot analysis indicated that MUC20 knockdown decreased HGF-mediated phosphorylation of MET in PDAC cells. Moreover, HGF-induced malignant phenotypes could be suppressed by MUC20 knockdown. Co-immunoprecipitation revealed the physical association of MUC20 and MET. These findings suggest that MUC20 knockdown suppresses the malignant phenotypes of PDAC cells at least partially through the inhibition of the HGF/MET pathway and that MUC20 could act as a potential therapeutic target.

Indexed as

AdenocarcinomaAnimalsCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansMaleMiceMice, Inbred NODMice, SCIDMiddle AgedMucinsPancreatic NeoplasmsHepatocyte Growth FactorHGF protein, humanMET protein, humanMUC20 protein, humanMucinsProto-Oncogene Proteins c-metRNA, Small Interfering

Identifiers

PMID29993037
PMCPMC6237765
OpenAlexW2876778388

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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.