Evidence map›Paper›PMID 32855524›Full record

ArticleOncogene2020

miR-21a in exosomes from Lewis lung carcinoma cells accelerates tumor growth through targeting PDCD4 to enhance expansion of myeloid-derived suppressor cells.

Xingju Zhang, Fei Li, Ying Tang, Qinglan Ren, Bin Xiao, Ying Wan, Shan Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 40 citations in OpenAlex.

  1. Exosome-mediated siRNA delivery in cancer: Loading strategies, targeting approaches, and therapeutic outcomes.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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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

7 authors at 4 institutions in 2 countries.

Xingju ZhangKey Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen, 518060, China.ORCID http://orcid.org/0000-0003-0717-2510
Fei LiBiomedical Analysis Center, Army Medical University, Chongqing, 400038, China.ORCID http://orcid.org/0000-0002-4695-944X
Ying TangKey Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen, 518060, China.
Qinglan RenDepartment of Oncology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Bin XiaoCollege of Pharmacy, Chongqing Medical University, Chongqing, 400016, China. binxiaotmmu@163.com.ORCID http://orcid.org/0000-0001-7159-4406
Ying WanBiomedical Analysis Center, Army Medical University, Chongqing, 400038, China. wanying516@foxmail.com.ORCID http://orcid.org/0000-0001-7922-4434
Shan JiangInstitute for Advanced Study, Shenzhen University, Shenzhen, 518060, China. shan.jiang1975@szu.edu.cn.ORCID http://orcid.org/0000-0002-8297-0099
Shenzhen University · CNArmy Medical University · CNChongqing Medical University · CNThe Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In patients with lung cancer, myeloid-derived suppressor cells (MDSCs) have been reported to be significantly increased. Tumor-derived exosomes (TDEs) from various cancers played a critical role in MDSC induction. However, studies on the molecular mechanism underlying MDSC expansion induced by exosomes from lung cancer cells are still limited. In this study, we demonstrated that LLC-Exo accelerated tumor growth along with a significant accumulation of MDSCs in mouse tumor model. miRNA profiling showed that miR-21a was enriched in LLC-Exo. The depletion of miR-21a in LLC-Exo leads to the loss of their ability to induce MDSC expansion. Further results showed that miR-21a of LLC-Exo induced MDSC expansion via downregulation of the programmed cell death protein 4 (PDCD4) protein. The results of gain-and loss-of-function experiments validated that PDCD4 function as a critical inhibitor to negatively regulate expansion of MDSCs via inhibition Il-6 production in bone marrow cells. In addition, our data showed that exosomes derived from human lung cancer cell lines expressing miR-21a, also induced expansion of MDSCs in human CD14

Indexed as

AnimalsApoptosis Regulatory ProteinsAutocrine CommunicationCarcinoma, Lewis LungCell Line, TumorCell ProliferationDown-RegulationExosomesFemaleGene Expression Regulation, NeoplasticGene Knockout TechniquesHealthy VolunteersHumansInterleukin-6Leukocytes, MononuclearMiceApoptosis Regulatory ProteinsInterleukin-6interleukin-6, mouseMicroRNAsMIRN21 microRNA, mousePdcd4 protein, mouseRNA-Binding ProteinsStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID32855524
OpenAlexW3080401878

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.