Evidence map›Paper›PMID 35459783›Full record

ArticleOncogene2022

Chemerin enhances mesenchymal features of glioblastoma by establishing autocrine and paracrine networks in a CMKLR1-dependent manner.

Jianqi Wu, Shuai Shen, Tianqi Liu, Xiufang Ren, Chen Zhu, Qingyu Liang, Xiao Cui, Ling Chen, Peng Cheng, Wen Cheng and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

29 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

11 authors at 3 institutions in 1 country.

Jianqi Wu *Department of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
Shuai Shen *Department of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
Tianqi Liu *Department of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
Xiufang RenDepartement of Pathology, Shengjing Hospital of China Medical University, Shenyang, China.
Chen ZhuDepartment of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
Qingyu LiangDepartment of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
Xiao CuiDepartment of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
Ling ChenDepartment of Neurosurgery, Chinese People's Liberation Army of China (PLA) General Hospital, Medical School of Chinese PLA, Institute of Neurosurgery of Chinese PLA, Beijing, China.
Peng ChengDepartment of Neurosurgery, The First Hospital of China Medical University, Shenyang, China.
Wen ChengDepartment of Neurosurgery, The First Hospital of China Medical University, Shenyang, China. cmu071207@163.com.ORCID http://orcid.org/0000-0003-0689-1695
Anhua WuDepartment of Neurosurgery, The First Hospital of China Medical University, Shenyang, China. ahwu@cmu.edu.cn.ORCID http://orcid.org/0000-0002-3402-1884
First Hospital of China Medical University · CNChina Medical University · CNChinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) with mesenchymal features exhibits enhanced chemotherapeutic resistance and results in reduced overall survival. Recent studies have suggested that there is a positive correlation between the GBM mesenchymal status and immune cell infiltration. However, the mechanisms by which GBM acquires its mesenchymal features in a tumor immune microenvironment-dependent manner remains unknown. Here, we uncovered a chemerin-mediated autocrine and paracrine network by which the mesenchymal phenotype of GBM cells is strengthened. We identified chemerin as a prognostic secretory protein mediating the mesenchymal phenotype-promoting network between tumor-associated macrophages (TAMs) and tumor cells in GBM. Mechanistically, chemerin promoted the mesenchymal features of GBM by suppressing the ubiquitin-proteasomal degradation of CMKLR1, a chemerin receptor predominantly expressed on TAMs and partially expressed on GBM cells, thereby enhancing NF-κB pathway activation. Moreover, chemerin was found to be involved in the recruitment of TAMs in the GBM tumor microenvironment. We revealed that chemerin also enhances the mesenchymal phenotype-promoting ability of TAMs and promotes their M2 polarization via a CMKLR1/NF-κB axis, which further exacerbates the mesenchymal features of GBM. Blocking the chemerin/CMKLR1 axis with 2-(α-naphthoyl) ethyltrimethylammonium iodide disrupted the mesenchymal network and suppressed tumor growth in GBM. These results suggest the therapeutic potential of targeting the chemerin/CMKLR1 axis to block the mesenchymal network in GBM.

Indexed as

GlioblastomaAutocrine CommunicationChemokinesHumansNF-kappa BParacrine CommunicationReceptors, ChemokineTumor-Associated MacrophagesTumor MicroenvironmentChemokinesCMKLR1 protein, humanNF-kappa BRARRES2 protein, humanReceptors, Chemokine

Identifiers

PMID35459783
PMCPMC9122825
OpenAlexW4224271830

What OpenQuestion holds

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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.