Evidence map›Paper›PMID 29713056›Full record

ArticleOncogene2018

Immunosuppressive effects of hypoxia-induced glioma exosomes through myeloid-derived suppressor cells via the miR-10a/Rora and miR-21/Pten Pathways.

Xiaofan Guo, Wei Qiu, Qinglin Liu, Mingyu Qian, Shaobo Wang, Zongpu Zhang, Xiao Gao, Zihang Chen, Hao Xue, Gang Li

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed
–field-weighted citation impact
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

196 citing papers in PubMed.

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136 more citing papers are in PubMed but not listed here.

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

10 authors.

Xiaofan GuoBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Wei QiuBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Qinglin LiuDepartment of Neurosurgery, Qilu Hospital of Shandong University, 107 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Mingyu QianBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Shaobo WangBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Zongpu ZhangBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Xiao GaoBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Zihang ChenBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China.
Hao XueBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China. undeadadams@163.com.
Gang LiBrain Science Research Institute, Shandong University, 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, P.R. China. ligangqiluhospital@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While immunosuppressive environments mediated by myeloid-derived suppressor cells (MDSCs) have been well documented in glioma patients, the mechanisms of MDSC development and activation have not been clearly defined. Here, we elucidated a role for glioma-derived exosomes (GDEs) in potentiating an MDSC pathway. We isolated normoxia-stimulated and hypoxia-stimulated GDEs and studied their MDSC induction abilities in vivo and in vitro. Analyses of spleen and bone marrow MDSC proportions (flow cytometry) and reactive oxygen species (ROS), arginase activity, nitric oxide (NO), T-cell proliferation and immunosuppressive cytokine (IL-10 and TGF-β, ELISA) levels were used to assess MDSC expansion and functional capacity. We also performed microRNA (miRNA) sequencing analysis of two types of GDEs to find miRNAs that potentially mediate the development and activation of MDSCs. GDE miRNA intracellular signaling in MDSCs was also studied. Hypoxia promoted the secretion of GDEs, and mouse MDSCs could uptake GDEs. Hypoxia-stimulated GDEs had a stronger ability to induce MDSCs than N-GDEs. The hypoxia-inducible expression of miR-10a and miR-21 in GDEs mediated GDE-induced MDSC expansion and activation by targeting RAR-related orphan receptor alpha (RORA) and phosphatase and tensin homolog (PTEN). Mice inoculated with miR-10a or miR-21 knockout glioma cells generated fewer MDSCs than those inoculated with normal glioma cells. These data elucidated a mechanism by which glioma cells influence the differentiation and activation of MDSCs via exosomes and demonstrated how local glioma hypoxia affects the entirety of tumor immune environments.

Indexed as

AnimalsCell Line, TumorExosomesGliomaHumansHypoxiaImmunosuppression TherapyInterleukin-10MaleMiceMice, Inbred C57BLMicroRNAsMyeloid CellsMyeloid-Derived Suppressor CellsNuclear Receptor Subfamily 1, Group F, Member 1PTEN PhosphohydrolaseInterleukin-10MicroRNAsNuclear Receptor Subfamily 1, Group F, Member 1PTEN Phosphohydrolase

Identifiers

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.