Evidence map›Paper›PMID 32943658›Full record

ArticleScientific reports2020

Downregulation of the CCL2/CCR2 and CXCL10/CXCR3 axes contributes to antitumor effects in a mouse model of malignant glioma.

Kenji Shono, Izumi Yamaguchi, Yoshifumi Mizobuchi, Hiroshi Kagusa, Akiko Sumi, Toshitaka Fujihara, Kohei Nakajima, Keiko T Kitazato, Kazuhito Matsuzaki, Hideyuki Saya and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 50 citations in OpenAlex.

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  7. Exploring G Protein-Coupled Receptors in Hematological Cancers.ACS pharmacology & translational science · 2024
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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

11 authors at 2 institutions in 1 country.

Kenji Shono *Department of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Izumi Yamaguchi *Department of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Yoshifumi MizobuchiDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan. y.mizobuchi1203@gmail.com.
Hiroshi KagusaDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Akiko SumiDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Toshitaka FujiharaDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Kohei NakajimaDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Keiko T KitazatoDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Kazuhito MatsuzakiDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research, School of Medicine, Keio University, Shinjuku-ku, Tokyo, 160-8582, Japan.ORCID http://orcid.org/0000-0001-6610-1902
Yasushi TakagiDepartment of Neurosurgery, Graduate School of Biomedical Sciences, Tokushima University, 3-18-15, Kuramoto-cho, Tokushima, 770-8503, Japan.
Tokushima University · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme involves glioma stem cells (GSCs) that are resistant to various therapeutic approaches. Here, we studied the importance of paracrine signaling in the glioma microenvironment by focusing on the celecoxib-mediated role of chemokines C-C motif ligand 2 (CCL2), C-X-C ligand 10 (CXCL10), and their receptors, CCR2 and CXCR3, in GSCs and a GSC-bearing malignant glioma model. C57BL/6 mice were injected with orthotopic GSCs intracranially and divided into groups administered either 10 or 30 mg/kg celecoxib, or saline to examine the antitumor effects associated with chemokine expression. In GSCs, we analyzed cell viability and expression of chemokines and their receptors in the presence/absence of celecoxib. In the malignant glioma model, celecoxib exhibited antitumor effects in a dose dependent manner and decreased protein and mRNA levels of Ccl2 and CxcL10 and Cxcr3 but not of Ccr2. CCL2 and CXCL10 co-localized with Nestin

Indexed as

AnimalsAntineoplastic AgentsCell LineChemokine CCL2Chemokine CXCL10Disease Models, AnimalDown-RegulationGliomaHumansMaleMiceMice, Inbred C57BLMicrogliaReceptors, CCR2Receptors, CXCR3Stem CellsAntineoplastic AgentsCCL2 protein, humanCCR2 protein, humanChemokine CCL2Chemokine CXCL10CXCL10 protein, humanCXCR3 protein, humanReceptors, CCR2Receptors, CXCR3

Identifiers

PMID32943658
PMCPMC7499211
OpenAlexW3087295802

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.