Evidence map›Paper›PMID 35440807›Full record

ArticleGene therapy2023

Exosomal PD-L1 confers chemoresistance and promotes tumorigenic properties in esophageal cancer cells via upregulating STAT3/miR-21.

Haojie Wang, Yijun Qi, Zijun Lan, Qiwei Liu, Juanjuan Xu, Mengxi Zhu, Tingting Yang, Ruolin Shi, Shegan Gao, Gaofeng Liang

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-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

24 citing papers in PubMed, 29 citations in OpenAlex.

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  11. Exosomes in esophageal cancer: function and therapeutic prospects.Medical oncology (Northwood, London, England) · 2024
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  15. FOXP4-AS1 promotes CD8Immunologic research · 2024
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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

10 authors at 3 institutions in 1 country.

Haojie WangSchool of Basic Medical Sciences, Henan University of Science & Technology, Luoyang, China.
Yijun QiHenan Key Laboratory of Microbiome and Esophageal Cancer Prevention and Treatment, The First Affiliated Hospital School of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Zijun LanHenan Key Laboratory of Microbiome and Esophageal Cancer Prevention and Treatment, The First Affiliated Hospital School of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Qiwei LiuKey Laboratory of Cell Behavior, Medical College of Xuchang University, Xuchang, China.
Juanjuan XuSchool of Basic Medical Sciences, Henan University of Science & Technology, Luoyang, China.
Mengxi ZhuSchool of Basic Medical Sciences, Henan University of Science & Technology, Luoyang, China.
Tingting YangSchool of Basic Medical Sciences, Henan University of Science & Technology, Luoyang, China.
Ruolin ShiSchool of Basic Medical Sciences, Henan University of Science & Technology, Luoyang, China.
Shegan GaoHenan Key Laboratory of Microbiome and Esophageal Cancer Prevention and Treatment, The First Affiliated Hospital School of Clinical Medicine of Henan University of Science and Technology, Luoyang, China. gsg112258@163.com.ORCID http://orcid.org/0000-0001-9055-1479
Gaofeng LiangSchool of Basic Medical Sciences, Henan University of Science & Technology, Luoyang, China. lgfeng990448@163.com.ORCID http://orcid.org/0000-0003-0097-0296
Henan University of Science and Technology · CNFirst Affiliated Hospital of Henan University of Science and Technology · CNXuchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy resistance remains a major obstacle in the treatment of esophageal cancer. Previous researches have shown that an increase in exosomal PD-L1 expression was positively associated with a more advanced clinical stage, a poorer prognosis as well as drug resistance in patients with esophageal squamous cell carcinoma (ESCC). To explore the role of exosomal PD-L1 in ESCC, we performed bioinformatics analysis as well as several in vitro/in vivo functional experiments in a parental sensitive cell line EC-9706 and its derivative, a paclitaxel-resistant subline EC-9706R, and found that the exosomal PD-L1 from EC-9706R was higher than that from EC-9706. Moreover, exosomes from EC-9706R significantly increased invasion, migration and chemoresistance of EC-9706. Anti-PD-L1 treatment in combination with chemotherapy also led to reduced tumor burden in vivo. Inhibition of the release of exosomes by GW4869 or inhibition of STAT3 phosphorylation by stattic could effectively reverse the resistance to paclitaxel mediated by exosomal PD-L1. Furthermore, we found that PD-L1, miR-21, and multidrug resistance (MDR1) gene are involved in the process of exosomal transfer. Moreover, PD-L1 could enhance miR-21 expression by increasing the enrichment of STAT3 on miR-21 promoter. Our results suggested that exosomal PD-L1 may contribute to drug resistance to paclitaxel by regulating the STAT3/miR-21/PTEN/Akt axis and promote tumorigenic phenotype. This study provides a novel potential therapeutic approach to reverse chemoresistance and tumor progression through exosomal PD-L1 in ESCC patients.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaExosomesMicroRNAsB7-H1 AntigenCell Line, TumorCell ProliferationDrug Resistance, NeoplasmHumansPaclitaxelSTAT3 Transcription FactorB7-H1 AntigenMicroRNAsMIRN21 microRNA, humanPaclitaxelSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID35440807
OpenAlexW4224230014

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.