Evidence map›Paper›PMID 35038580›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022

Exosome-derived circTRPS1 promotes malignant phenotype and CD8+ T cell exhaustion in bladder cancer microenvironments.

Chen Yang, Siqi Wu, Zezhong Mou, Quan Zhou, Xiyu Dai, Yuxi Ou, Xinan Chen, Yiling Chen, Chenyang Xu, Yun Hu and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 3 pooled it
14.7field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 3 syntheses or guidelines pooled it, 174 citations in OpenAlex.

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47 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

16 authors at 2 institutions in 1 country.

Chen YangDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Fudan University, Shanghai, China. Electronic address: yangc_huashan@163.com.
Siqi WuDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Zezhong MouDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Quan ZhouDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Xiyu DaiDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Yuxi OuDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Xinan ChenDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Yiling ChenDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Chenyang XuDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Yun HuDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Limin ZhangDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Lujia ZouDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China.
Shengming JinDepartment of Urology, Fudan University Shanghai Cancer Center, Shanghai, China.
Jimeng HuDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China. Electronic address: jimeng1214@126.com.
Shanhua MaoDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China. Electronic address: maoshanhua@163.com.
Haowen JiangDepartment of Urology, Huashan Hospital, Fudan University, Shanghai, China; Fudan Institute of Urology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Fudan University, Shanghai, China. Electronic address: haowj_sh@fudan.edu.cn.
Fudan University · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circular RNAs (circRNAs) play critical roles in different diseases. Exosomes are important intermediates of intercellular communication. While both have been widely reported in cancers, exosome-derived circRNAs are rarely studied. In this work, we identified the differently expressed circRNAs in bladder cancer (BCa) tissue and exosomes through high-throughput sequencing. RNA pull-down, RNA immunoprecipitation, and luciferase reporter assays were used to investigate the interactions between specific circRNAs, microRNAs (miRNAs), and mRNAs. Wound-healing, Transwell, Cell Counting Kit-8 (CCK8), and colony-formation assays were used to study the biological roles in vitro. Metabolomics were used to explore the mechanism of how specific circRNAs influenced BCa cell behavior. Flow cytometry was used to study how specific circRNAs affected the function of CD8+ T cells in tumor microenvironments. We identified that exosome-derived hsa_circ_0085361 (circTRPS1) was correlated with aggressive phenotypes of BCa cells via sponging miR-141-3p. Metabolomics and RNA sequencing (RNA-seq) identified GLS1-mediated glutamine metabolism was involved in circTRPS1-mediated alterations. Exosomes derived from circTRPS1 knocked down BCa cells, prevented CD8+ T cells from exhaustion, and repressed the malignant phenotype of BCa cells. In conclusion, exosome-derived circTRPS1 from BCa cells can modulate the intracellular reactive oxygen species (ROS) balance and CD8+ T cell exhaustion via the circTRPS1/miR141-3p/GLS1 axis. Our work may provide a potential biomarker and therapeutic target for BCa.

Indexed as

ExosomesMicroRNAsNeoplasmsCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansPhenotypeRNA, CircularTumor MicroenvironmentUrinary BladderMicroRNAsRNA, Circularbladder cancerCD8+ T cellcircular RNAsexosomesROStumor microenvironment

Identifiers

PMID35038580
PMCPMC8899700
OpenAlexW4206477728

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.