Evidence map›Paper›PMID 31505062›Full record

ArticleCancer science2019

E-cadherin-Fc chimera protein matrix enhances cancer stem-like properties and induces mesenchymal features in colon cancer cells.

Yamin Qian, Xin Wu, Yuhki Yokoyama, Daisuke Okuzaki, Mai Taguchi, Haruka Hirose, Jiaqi Wang, Tsuyoshi Hata, Akira Inoue, Masayuki Hiraki and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Review
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  11. Proteolytic Landscapes in Gastric Pathology and Cancerogenesis.International journal of molecular sciences · 2022
    Review
  12. Functional assessment of miR‑1291 in colon cancer cells.International journal of oncology · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. 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

17 authors at 4 institutions in 1 country.

Yamin QianDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Xin WuDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Yuhki YokoyamaDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Mai TaguchiDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Haruka HiroseDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Jiaqi WangDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tsuyoshi HataDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Akira InoueDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Masayuki HirakiDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Masahisa OhtsukaDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Hidekazu TakahashiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Naotsugu HaraguchiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tsunekazu MizushimaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Shinji TanakaDepartment of Molecular Oncology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-7718-3453
Masaki MoriDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Hirofumi YamamotoDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, Osaka, Japan.
Osaka Health Science University · JPThe University of Osaka · JPKyushu University · JPTokyo Medical and Dental University · JP

Funding

Kagoshima Shinsangyo Sousei Investment Limited PartnershipRotary Yoneyama Memorial Foundation RY036688
6 · The paper itself

Abstract

Cancer stem cells (CSC) are a subpopulation of tumor cells with properties of high tumorigenicity and drug resistance, which lead to recurrence and poor prognosis. Although a better understanding of CSC is essential for developing cancer therapies, scarcity of the CSC population has hindered such analyses. The aim of the present study was to elucidate whether the E-cadherin-Fc chimera protein (E-cad-Fc) enhances cancer stem-like properties because studies show that soluble E-cadherin stimulates human epithelial growth factor receptor (EGFR) and downstream signaling pathways that are reported to play a crucial role in CSC. For this purpose, we used ornithine decarboxylase (ODC)-degron-transduced (Degron(+)) KM12SM cells as a CSC model that retains relatively low CSC properties. Compared to cultures without E-cad-Fc treatment, we found that E-cad-Fc treatment further suppressed proteasome activity and largely enhanced cancer stem-like properties of ODC-degron-transduced KM12SM cells. These results include increased expression of stem cell markers Lgr5, Bmi-1, SOX9, CD44, and CD44v9, aldehyde dehydrogenase (ALDH), and enhancement of robust spheroid formation, and chemoresistance to 5-fluorouracil (5-FU) and oxaliplatin (L-OHP). These effects could be attributed to activation of the EGFR pathway as identified by extensive phosphorylation of EGFR, ERK, PI3K, AKT, and mTOR. In SW480 cells, E-cad-Fc matrix induced some CSC markers such as CD44v9 and ALDH. We also found that E-cad-Fc matrix showed high efficiency of inducing mesenchymal changes in colon cancer cells. Our data suggest that the E-cad-Fc matrix may enhance CSC properties such as enhancement of chemoresistance and sphere formation.

Indexed as

ErbB ReceptorsImmunoglobulin Fc FragmentsAldehyde DehydrogenaseAntineoplastic AgentsCell Line, TumorColonic NeoplasmsDrug Resistance, NeoplasmFluorouracilHumansHyaluronan ReceptorsNeoplastic Stem CellsOrnithine DecarboxylaseOxaliplatinPolycomb Repressive Complex 1Proteasome Endopeptidase ComplexReceptors, G-Protein-CoupledAldehyde DehydrogenaseAntineoplastic AgentsBMI1 protein, humanCD44 protein, humanErbB ReceptorsFluorouracilHyaluronan ReceptorsImmunoglobulin Fc FragmentsLGR5 protein, humanOrnithine DecarboxylaseOxaliplatinPolycomb Repressive Complex 1Proteasome Endopeptidase ComplexReceptors, G-Protein-CoupledRecombinant Fusion ProteinsSOX9 protein, humanSOX9 Transcription Factorcancer stem cellcolon cancerE-cadherin-Fcepithelial-mesenchymal transitionextracellular matrix

Identifiers

PMID31505062
PMCPMC6825015
OpenAlexW2972914310

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.