Evidence map›Paper›PMID 36631876›Full record

ArticleBiology direct2023

M2 macrophage-derived exosomal miR-193b-3p promotes progression and glutamine uptake of pancreatic cancer by targeting TRIM62.

Ke Zhang, Yu-Jie Li, Lin-Jia Peng, Hui-Feng Gao, Lu-Ming Liu, Hao Chen

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

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  12. Small extracellular vesicles (sEVs) in pancreatic cancer progression and diagnosis.Journal of controlled release : official journal of the Controlled Release Society · 2025
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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

6 authors at 2 institutions in 1 country.

Ke ZhangDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, No.270 DongAn Road, Shanghai, 200032, China.
Yu-Jie LiDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, No.270 DongAn Road, Shanghai, 200032, China.
Lin-Jia PengDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, No.270 DongAn Road, Shanghai, 200032, China.
Hui-Feng GaoDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, No.270 DongAn Road, Shanghai, 200032, China.
Lu-Ming LiuDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, No.270 DongAn Road, Shanghai, 200032, China.
Hao ChenDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, No.270 DongAn Road, Shanghai, 200032, China. chengkll@sina.com.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China 81973616
6 · The paper itself

Abstract

backgroundPancreatic cancer (PC) is a highly lethal malignancy that requires effective novel therapies. M2 macrophages are abundant in the PC microenvironment and promote cancer progression. Exosomes are emerging mediators of the crosstalk between cancer cells and the microenvironment. This study was conducted to explore the role of M2 macrophage-derived exosomes in PC.

methodsExosomes derived from M2 macrophages were extracted. miR-193b-3p and TRIM62 were overexpressed or silenced to examine their function in PC. Luminescence assays were used to investigate the interaction between miR-193b-3p and TRIM62. Cell proliferation was examined by EdU staining. Would healing and transwell assays were applied to evaluate cell migration and invasion. Co-immunoprecipitation was used to assess the interaction between TRIM62 and c-Myc. Gene and protein expressions were analyzed by quantitative RT-PCR and immunoblotting, respectively.

resultsM2 macrophage-derived exosomal miR-193b-3p promoted the proliferation, migration, invasion, and glutamine uptake of SW1990 cells. Mechanism study revealed that TRIM62 is a target of miR-193b-3p. TRIM62 inhibited the proliferation, migration, invasion, and glutamine uptake of SW1990 cells by promoting c-Myc ubiquitination. Our data also suggested that TRIM62 expression negatively correlated with miR-193b-3p and c-Myc expression. High-expression of miR-193b-3p and c-Myc predicts poor prognosis, whereas low-expression of TRIM62 predicts poor prognosis in patients with PC.

conclusionM2 macrophage-derived exosomal miR-193b-3p enhances the proliferation, migration, invasion, and glutamine uptake of PC cells by targeting TRIM62, resulting in the decrease of c-Myc ubiquitination. This study not only reveals the mechanism underlying the crosstalk between M2 macrophages and PC cells but also suggests a promising therapeutic target for PC.

Indexed as

ExosomesMicroRNAsPancreatic NeoplasmsCell Line, TumorCell ProliferationGlutamineHumansMacrophagesTumor MicroenvironmentGlutamineMicroRNAsExosomeGlutamine metabolismMacrophageMiRNAPancreatic cancer

Identifiers

PMID36631876
PMCPMC9832623
OpenAlexW4315648407

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.