Evidence map›Paper›PMID 20101228›Full record

ArticleOncogene2010

Osteopontin-mediated enhanced hyaluronan binding induces multidrug resistance in mesothelioma cells.

K Tajima, R Ohashi, Y Sekido, T Hida, T Nara, M Hashimoto, S Iwakami, K Minakata, T Yae, F Takahashi and 2 more

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01590472 (Consortium for the Sharing of Germ Line DNA and Tissue From Subjects With Mesothelioma), which is not on this map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 12% 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.

NCT01590472 completednot on this mapstarted 2011, after this paper: background citation

Consortium for the Sharing of Germ Line DNA and Tissue From Subjects With Mesothelioma

TypeobservationalSponsorWake Forest UniversityRan2011 to 2015Enrolled69ConditionsMesothelioma
3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Hyaluronan synthesis is necessary for autoreactive T-cell trafficking, activation, and Th1 polarization.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Prognostic value of several biomarkers for the patients with malignant pleural mesothelioma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Multiple myeloma mesenchymal stem cells: characterization, origin, and tumor-promoting effects.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    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

12 authors at 5 institutions in 1 country.

K TajimaDepartment of Respiratory Medicine, Juntendo University, School of Medicine, Bunkyo-Ku, Tokyo, Japan. tajiken@juntendo.ac.jp
R Ohashi
Y Sekido
T Hida
T Nara
M Hashimoto
S Iwakami
K Minakata
T Yae
F Takahashi
H Saya
K Takahashi
Juntendo University · JPAichi Cancer Center · JPJuntendo University Hospital · JPJuntendo University Shizuoka Hospital · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant pleural mesothelioma (MPM) is resistant to chemotherapy and thus shows a dismal prognosis. Osteopontin (OPN), a secreted noncollagenous and phosphoprotein, is suggested to be involved in the pathogenesis of MPM. However, the precise role of OPN, especially in the multidrug resistance of MPM, remains to be elucidated. We therefore established stable transfectants (ACC-MESO-1/OPN), which constitutively express OPN, to determine its role in the chemoresistance observed in MPM. The introduction of the OPN gene provides MPM cells with upregulated multidrug resistance through the mechanism of enhanced hyaluronate (HA) binding. The expression of CD44 variant isoforms, which inhibit HA binding, significantly decreased in ACC-MESO-1/OPN cells in comparison to control transfectants. Interestingly, the inhibition of the HA-CD44 interaction abrogated multidrug resistance in the ACC-MESO-1/OPN, thus suggesting the involvement of the surviving signal emanating from the HA-CD44 interaction. An enhanced level of the p-Akt in ACC-MESO-1/OPN cells was observed, and was diminished by CD44 siRNA. Inhibition of the Akt phosphorylation increased in number of the cells underwent apoptosis induced by NVB, VP-16 and GEM. Collectively, these results indicate that OPN is strongly involved in multidrug resistance by enhancing the CD44 binding to HA.

Indexed as

Antineoplastic AgentsCell AdhesionCell Line, TumorDrug Resistance, MultipleDrug Resistance, NeoplasmEtoposideGene Expression Regulation, NeoplasticHumansHyaluronic AcidMesotheliomaOsteopontinPleural NeoplasmsRNA, Small InterferingSignal TransductionAntineoplastic AgentsEtoposideHyaluronic AcidOsteopontinRNA, Small Interfering

Identifiers

PMID20101228
OpenAlexW2084608986

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.