Evidence map›Paper›PMID 24466195›Full record

ArticlePloS one2014

CD9 negatively regulates CD26 expression and inhibits CD26-mediated enhancement of invasive potential of malignant mesothelioma cells.

Toshihiro Okamoto, Satoshi Iwata, Hiroto Yamazaki, Ryo Hatano, Eriko Komiya, Nam H Dang, Kei Ohnuma, Chikao Morimoto

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. 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
1.3field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. A Systems Biology Approach Unveils a Critical Role of DPP4 in Upper Gastrointestinal Cancer Patient Outcomes.Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer · 2024
    Article
  3. CD26Frontiers in immunology · 2023
    Article
  4. CD9, a tetraspanin target for cancer therapy?Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  5. Article
  6. Review
  7. The Roles of Integrin α5β1 in Human Cancer.OncoTargets and therapy · 2020
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Suppression of CD26 inhibits growth and metastasis of pancreatic cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  18. DPPIV/CD26: a tumor suppressor or a marker of malignancy?Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  19. Article
  20. 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 3 institutions in 2 countries.

Toshihiro OkamotoDepartment of Therapy Development and Innovation for Immune disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan ; Division of Clinical Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Satoshi IwataDepartment of Therapy Development and Innovation for Immune disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan ; Division of Clinical Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Hiroto YamazakiDepartment of Therapy Development and Innovation for Immune disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan ; Division of Clinical Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Ryo HatanoDepartment of Therapy Development and Innovation for Immune disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan ; Division of Clinical Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Eriko KomiyaDepartment of Therapy Development and Innovation for Immune disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Nam H DangDivision of Hematology and Oncology, University of Florida Shands Cancer Center, Gainesville, Florida, United States of America.
Kei OhnumaDepartment of Therapy Development and Innovation for Immune disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan ; Division of Clinical Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Chikao MorimotoDepartment of Therapy Development and Innovation for Immune disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan ; Division of Clinical Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Juntendo University · JPTokyo University of Science · JPUF Health Cancer Center

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD26/dipeptidyl peptidase IV is a cell surface glycoprotein which consists of multiple functional domains beside its ectopeptidase site. A growing body of evidence indicates that elevated expression of CD26 correlates with disease aggressiveness and invasive potential of selected malignancies. To further explore the molecular mechanisms involved in this clinical behavior, our current work focused on the interaction between CD26 and CD9, which were recently identified as novel markers for cancer stem cells in malignant mesothelioma. We found that CD26 and CD9 co-modulated and co-precipitated with each other in the malignant mesothelioma cell lines ACC-MESO1 and MSTO-211H. SiRNA study revealed that depletion of CD26 led to increased CD9 expression, while depletion of CD9 resulted in increased CD26 expression. Consistent with these findings was the fact that gene transfer of CD26 into CD26-negative MSTO-211H cells reduced CD9 expression. Cell invasion assay showed that overexpression of CD26 or gene depletion of CD9 led to enhanced invasiveness, while CD26 gene depletion resulted in reduced invasive potential. Furthermore, our work suggested that this enhanced invasiveness may be partly mediated by α5β1 integrin, since co-precipitation studies demonstrated an association between CD26 and α5β1 integrin. Finally, gene depletion of CD9 resulted in elevated protein levels and tyrosine phosphorylation of FAK and Cas-L, which are downstream of β1 integrin, while depletion of CD26 led to a reduction in the levels of these molecules. Collectively, our findings suggest that CD26 potentiates tumor cell invasion through its interaction with α5β1 integrin, and CD9 negatively regulates tumor cell invasion by reducing the level of CD26-α5β1 integrin complex through an inverse correlation between CD9 and CD26 expression. Our results also suggest that CD26 and CD9 serve as potential biomarkers as well as promising molecular targets for novel therapeutic approaches in malignant mesothelioma and other malignancies.

Indexed as

Cell MovementCell ProliferationAnimalsApoptosisBlotting, WesternCell MembraneDipeptidyl Peptidase 4FemaleFlow CytometryHumansImmunoprecipitationIntegrin beta1Lung NeoplasmsMesotheliomaMesothelioma, MalignantMiceCD9 protein, humanDipeptidyl Peptidase 4DPP4 protein, humanIntegrin beta1RNA, MessengerRNA, Small InterferingTetraspanin 29

Identifiers

PMID24466195
PMCPMC3900581
OpenAlexW1980571380

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.