Evidence map›Paper›PMID 35410993›Full record

ArticleCell death discovery2022

Suppression of the hyaluronic acid pathway induces M1 macrophages polarization via STAT1 in glioblastoma.

Tao Yan, Kaikai Wang, Jiafeng Li, Hong Hu, He Yang, Meng Cai, Ruijie Liu, Honglei Li, Ning Wang, Ying Shi and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-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

15 citing papers in PubMed, 31 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.

Tao Yan *Department of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Kaikai Wang *Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Jiafeng Li *Department of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Hong Hu *Department of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China.
He YangDepartment of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Meng CaiDepartment of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Ruijie LiuDepartment of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Honglei LiDepartment of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Ning WangDepartment of Critical Care Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Ying ShiDepartment of Radiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Wei HuaDepartment of Pathology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Huailei LiuDepartment of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin, China. liuhuaileinsdm@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-0766-4809
Harbin Medical University · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) NO.82002634
6 · The paper itself

Abstract

Immunosuppressive tumor microenvironment is a crucial factor that impedes the success of tumor immunotherapy, and tumor-associated macrophages (TAMs) are essential for the formation of tumor immunosuppressive microenvironment. Hyaluronic acid (HA) is highly important brick for glioblastoma microenvironment, but whether it contributes to TAM polarization and glioblastoma immunosuppressive microenvironment is less well known. In our study, we observed that disrupting glioblastoma HA synthesis or blocking HA binding to its receptor CD44 on macrophages increased the proportion of M1 macrophages by upregulating SIRPα in macrophages, the underlying mechanism was elevated SIRPα enhanced STAT1 phosphorylation and suppressed STAT3 phosphorylation in macrophages. Subsequently, the induced macrophages could inhibit glioblastoma growth via a feedback effect. In addition, 4-methylumbelliferone (4MU), a cholecystitis drug, can disrupt the CD47/SIRPα axis by disturbing glioblastoma HA synthesis. Collectively, these findings indicated that HA plays a crucial role in macrophages polarization and CD47/SIRPα signaling between glioblastoma cells and macrophages, and suppressing the HA pathway may be a new immunotherapeutic approach for glioblastoma.

Identifiers

PMID35410993
PMCPMC9001679
OpenAlexW4223610540

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.