Evidence map›Paper›PMID 34591282›Full record

ArticleHuman cell2022

Macrophage/microglia-derived IL-1β induces glioblastoma growth via the STAT3/NF-κB pathway.

Keitaro Kai, Yoshihiro Komohara, Shigeyuki Esumi, Yukio Fujiwara, Takahiro Yamamoto, Ken Uekawa, Kazutaka Ohta, Tatsuya Takezaki, Junichiro Kuroda, Naoki Shinojima and 2 more

Open access · goldAbstract read
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In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Keitaro KaiDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan. ycomo@kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0001-9723-0846
Shigeyuki EsumiDepartment of Morphological Neural Science, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Yukio FujiwaraDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto Chuo-ku, Kumamoto, 860-8556, Japan.
Takahiro YamamotoDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Ken UekawaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Kazutaka OhtaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Tatsuya TakezakiDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Junichiro KurodaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Naoki ShinojimaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Tadashi HamasakiDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Akitake MukasaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Kumamoto University · JPKumamoto Health Science University · JP

Funding

Japan Society for the Promotion of Science 20H03459Japan Society for the Promotion of Science 20H03792
6 · The paper itself

Abstract

Glioblastoma is a glioma characterized by highly malignant features. Numerous studies conducted on the relationship between glioblastoma and the microenvironment have indicated the significance of tumor-associated macrophages/microglia (TAMs) in glioblastoma progression. Since interleukin (IL)-1β secreted by TAMs has been suggested to promote glioblastoma growth, we attempted to elucidate the detailed mechanisms of IL-1β in glioblastoma growth in this study. A phospho-receptor tyrosine kinase array and RNA-sequencing studies indicated that IL-1β induced the activation of signal transducer and activator of transcription-3 and nuclear factor-kappa B signaling. Glioblastoma cells stimulated by IL-1β induced the production of IL-6 and CXCL8, which synergistically promoted glioblastoma growth via signal transducer and activator of transcription-3 and nuclear factor-kappa B signaling. By immunohistochemistry, IL-1β expression was seen on TAMs, especially in perinecrotic areas. These results suggest that IL-1β might be a useful target molecule for anti-glioblastoma therapy.

Indexed as

Brain NeoplasmsCell LineGene ExpressionGlioblastomaHumansInterleukin-1betaMacrophagesMicrogliaMolecular Targeted TherapyNF-kappa BSignal TransductionSTAT3 Transcription FactorInterleukin-1betaNF-kappa BSTAT3 protein, humanSTAT3 Transcription FactorCXCL8GlioblastomaIL-1βIL-6Macrophage

Identifiers

PMID34591282
OpenAlexW3201983294

What OpenQuestion holds

Textmetadata
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.