Evidence map›Paper›PMID 38459596›Full record

ArticleMolecular cancer2024

Exosome circATP8A1 induces macrophage M2 polarization by regulating the miR-1-3p/STAT6 axis to promote gastric cancer progression.

Cuncan Deng, Mingyu Huo, Hongwu Chu, Xiaomei Zhuang, Guofei Deng, Wenchao Li, Hongfa Wei, Leli Zeng, Yulong He, Huashan Liu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 1 pooled it
30.4field-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

126 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

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  18. Mycobacterium tuberculosis reinforces M2 polarization of macrophages by activating glutamine metabolism.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026
    Article
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66 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

13 authors at 3 institutions in 1 country.

Cuncan Deng *Digestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Mingyu Huo *Digestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Hongwu Chu *Digestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Xiaomei Zhuang *Digestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Guofei DengDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Wenchao LiDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Hongfa WeiDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Leli ZengDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China. Zenglli6@mail.sysu.edu.cn.
Yulong HeDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Huashan LiuDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Jia LiDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China. lijia88@mail.sysu.edu.cn.
Changhua ZhangDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China. zhchangh@mail.sysu.edu.cn.
Hengxing ChenDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China. chenhx49@mail2.sysu.edu.cn.
The Seventh Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CNSixth Affiliated Hospital of Sun Yat-sen University · CN

Funding

China Postdoctoral Science Foundation 2022M713588 and 2023M744016Guangdong Provincial Key Laboratory of Digestive Cancer Research 2021B1212040006Sanming Project of Medicine in Shenzhen SZSM201911010Shenzhen Excellent Science and Technology Innovation Talent Training Project RCBS20210706092410024 and JCYJ20220530144815035Shenzhen Key Medical Discipline Construction Fund SZXK016the National Natural Science Foundation of China U20A20379, 82220108013, 82073148, 82200569 and 82102716
6 · The paper itself

Abstract

Circular RNAs (circRNAs) play important roles in gastric cancer progression but the regulatory role of circRNAs in controlling macrophage function remains elusive. Exosomes serve as cargo for circRNAs and play a crucial role as mediators in facilitating communication between cancer cells and the tumor microenvironment. In this study, we found that circATP8A1, a previously unreported circular RNA, is highly expressed in both gastric cancer tissues and exosomes derived from plasma. Increased circATP8A1 was associated with advanced TNM stage and worse prognosis in patients with gastric cancer. We showed that  the circATP8A1 knockdown significantly inhibited gastric cancer proliferation and invasion in vitro and in vivo. Functionally, exosome circATP8A1 induced the M2 polarization of macrophages through the STAT6 pathway instead of the STAT3 pathway. Mechanistically, circATP8A1 was shown to activate the STAT6 pathway through competitive binding to miR-1-3p, as confirmed by Fluorescence In Situ Hybridization (FISH), RNA immunoprecipitation, RNA pulldown, and Luciferase reporter assays. The reversal of circATP8A1-induced STAT6 pathway activation and macrophage polarization was observed upon blocking miR-1-3p. Macrophages treated with exosomes from gastric cancer cells overexpressing circATP8A1 were able to promote gastric cancer migration, while knockdown of circATP8A1 reversed these effects in vivo. In summary, exosome-derived circATP8A1 from gastric cancer cells induce macrophages M2 polarization via the circATP8A1/miR-1-3p/STAT6 axis, and tumor progression. Our results highlight circATP8A1 as a potential prognostic biomarker and therapeutic target in gastric cancer.

Indexed as

ExosomesMicroRNAsStomach NeoplasmsAdenosine TriphosphatasesCell Line, TumorCell ProliferationHumansIn Situ Hybridization, FluorescenceMacrophagesPhospholipid Transfer ProteinsRNA, CircularSTAT6 Transcription FactorTumor MicroenvironmentAdenosine TriphosphatasesATP8A1 protein, humanMicroRNAsMIRN1 microRNA, humanPhospholipid Transfer ProteinsRNA, CircularSTAT6 protein, humanSTAT6 Transcription FactorExosomesGastric cancerM2 polarizationMacrophagesSTAT6

Identifiers

PMID38459596
PMCPMC10921793
OpenAlexW4392596657

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.