Evidence map›Paper›PMID 30171204›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2018

Endogenous and exogenous galectin-3 promote the adhesion of tumor cells with low expression of MUC1 to HUVECs through upregulation of N-cadherin and CD44.

Zhanqi Cao, Zhaojun Hao, Ming Xin, Lugang Yu, Lei Wang, Ying Zhang, Xinke Zhang, Xiuli Guo

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023
    Review
  9. Article
  10. Article
  11. 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

8 authors at 2 institutions in 2 countries.

Zhanqi CaoDepartment of Pharmacology Drug Screening Platform of Shandong Province Center for Drug R&D, School of Pharmaceutical Sciences, Shandong University, 250012, Jinan, China.
Zhaojun HaoDepartment of Pharmacology Drug Screening Platform of Shandong Province Center for Drug R&D, School of Pharmaceutical Sciences, Shandong University, 250012, Jinan, China.
Ming XinDepartment of Pharmacology Drug Screening Platform of Shandong Province Center for Drug R&D, School of Pharmaceutical Sciences, Shandong University, 250012, Jinan, China.
Lugang YuDepartment of Gastroenterology, Institute of Translational Medicine, University of Liverpool, Liverpool, L69 3GE, UK.
Lei WangDepartment of Pharmacology Drug Screening Platform of Shandong Province Center for Drug R&D, School of Pharmaceutical Sciences, Shandong University, 250012, Jinan, China.
Ying ZhangDepartment of Pharmacology Drug Screening Platform of Shandong Province Center for Drug R&D, School of Pharmaceutical Sciences, Shandong University, 250012, Jinan, China.
Xinke ZhangDepartment of Pharmacology Drug Screening Platform of Shandong Province Center for Drug R&D, School of Pharmaceutical Sciences, Shandong University, 250012, Jinan, China.
Xiuli GuoDepartment of Pharmacology Drug Screening Platform of Shandong Province Center for Drug R&D, School of Pharmaceutical Sciences, Shandong University, 250012, Jinan, China. guoxl@sdu.edu.cn.
Shandong University · CNUniversity of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cell-endothelial adhesion is one of the key steps in tumor cell haematogenous dissemination in metastasis and was previously shown to be mediated by interaction of galectin-3 with the transmembrane mucin protein MUC1. In this study, the effect of exogenous as well as endogenous galectin-3 on adhesion of two cell lines (low MUC1-expressing human prostate cancer PC-3M cells and non-small-cell lung cancer A549 cells) to monolayer of umbilical vein endothelial cells (HUVECs) was investigated. We found that suppression of endogenous galectin-3 expression reduced tumor cell adhesion to HUVECs and also decreased cell invasion and migration. Exogenous galectin-3 promoted tumor cell adhesion to HUVECs by entering cells. Both exogenous and endogenous galectin-3 upregulated the expression of β-catenin and increased β-catenin nuclear accumulation, and subsequently upregulated the expression of N-cadherin and CD44. We deduced that both exogenous as well as endogenous galectin-3 promoted low MUC1-expressing cancer cell adhesion to HUVECs by increasing the expression of N-cadherin and CD44 via an increase of nuclear β-catenin accumulation. These results were confirmed further by using a β-catenin/TCF transcriptional activity inhibitor, N-cadherin or CD44 siRNAs. Taken together, our results suggest a new molecular mechanism of galectin-3-mediated cell adhesion in cancer metastasis.

Indexed as

CadherinsCell AdhesionGalectin 3Gene Expression Regulation, NeoplasticHyaluronan ReceptorsA549 CellsAnimalsbeta CateninCell MovementFemaleHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred BALB CMice, NudeMucin-1beta CateninCadherinsCD44 protein, humanGalectin 3Hyaluronan ReceptorsMUC1 protein, humanMucin-1

Identifiers

PMID30171204
OpenAlexW2889188914

What OpenQuestion holds

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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.