Evidence map›Paper›PMID 33452462›Full record

ArticleOncogene2021

BATF2 prevents glioblastoma multiforme progression by inhibiting recruitment of myeloid-derived suppressor cells.

Xin Zhang, Yi Liu, Lei Dai, Gang Shi, Jie Deng, Qiang Luo, Qian Xie, Lin Cheng, Chunlei Li, Yi Lin and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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  17. Blood RNA Sequencing Indicates UpregulatedInternational journal of molecular sciences · 2022
    Article
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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

21 authors at 2 institutions in 1 country.

Xin Zhang *State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Yi Liu *State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Lei Dai *State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Gang ShiState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Jie DengState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Qiang LuoHuaxi MR Research Center, Department of Radiology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China.
Qian XieGeneral Practice Department of West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China.
Lin ChengState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Chunlei LiState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Yi LinState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Qingnan WangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Ping FanHuaxi Biobank, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China.
Hantao ZhangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Xiaolan SuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Shuang ZhangCancer Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China.
Yang YangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Xun HuHuaxi Biobank, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China.
Qiyong GongHuaxi MR Research Center, Department of Radiology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China.ORCID http://orcid.org/0000-0002-5912-4871
Dechao YuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China.
Lei ZhengLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, PR China. nfyyzhenglei@smu.edu.cn.ORCID http://orcid.org/0000-0003-2576-8780
Hongxin DengState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China. denghongx@scu.edu.cn.ORCID http://orcid.org/0000-0001-5094-1376
Sichuan University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The basic leucine zipper ATF-like transcription factor 2 (BATF2) has been implicated in inflammatory responses and anti-tumour effects. Little, however, is known regarding its extracellular role in maintaining a non-supportive cancer microenvironment. Here, we show that BATF2 inhibits glioma growth and myeloid-derived suppressor cells (MDSCs) recruitment. Interestingly, extracellular vesicles (EVs) from BATF2-overexpressing glioma cell lines (BATF2-EVs) inhibited MDSCs chemotaxis in vitro. Moreover, BATF2 inhibited intracellular SDF-1α and contributes to decreased SDF-1α in EVs. In addition, BATF2 downregulation-induced MDSCs recruitment were reversed by blocking SDF-1α/CXCR4 signalling upon AMD3100 treatment. Specifically, detection of EVs in 24 pairs of gliomas and healthy donors at different stages revealed that the abundance of BATF2-positive EVs in plasma (BATF2

Indexed as

AdultAgedAnimalsBasic-Leucine Zipper Transcription FactorsBenzylaminesCell Line, TumorCell Migration InhibitionChemokine CXCL12CyclamsFemaleGene Expression Regulation, NeoplasticGlioblastomaHeterograftsHumansMaleMiceBasic-Leucine Zipper Transcription FactorsBatf2 protein, humanBenzylaminesChemokine CXCL12CXCR4 protein, humanCyclamsplerixaforReceptors, CXCR4Tumor Suppressor Proteins

Identifiers

PMID33452462
PMCPMC7906906
OpenAlexW3121832200

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.