Evidence map›Paper›PMID 40448098›Full record

ArticleBMC cancer2025

CircSLC22A3 inhibits the invasion and metastasis of ESCC via the miR-19b-3p/TRAK2 axis and by reducing the stability of m

Yingjie Pan, Hang Yang, Jiayi Zhang, Ruolan Zhang, Yun Liu, Jun Bie, Qiaoling Chen, Yan Qiao, Kang Liu, Guiqin Song

Abstract read
In one paragraph

Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Yingjie PanInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China.
Hang YangInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China.
Jiayi ZhangInstitute of Basic Medicine and Forensic Medicine, North Sichuan Medical College, Nanchong, 637100, P.R. China.
Ruolan ZhangInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China.
Yun LiuInstitute of Basic Medicine and Forensic Medicine, North Sichuan Medical College, Nanchong, 637100, P.R. China.
Jun BieInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China.
Qiaoling ChenInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China.
Yan QiaoInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China.
Kang LiuInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China. liukang@nsmc.edu.cn.
Guiqin SongInstitute of Tissue Engineering and Stem Cell Research, The Second Clinical College of North Sichuan Medical College, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, 637000, P.R. China. songguiqin@nsmc.edu.cn.

Funding

Doctoral Fund of North Sichuan Medical College CBY22-QDA01Scientific Research Project of Nanchong Science and Technology Bureau 23JCYJPT0028Sichuan Provincial Healthcare Commission Popularization and Application Project 21PJ194Sichuan Provincial Science and Technology Department Seedling Project MZGC20240071 & MZGC20240072The Fund of North Sichuan Medical College CBY23-ZDA11the Natural Science Foundation of China 82203851
6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinoma (ESCC) is a major contributor to cancer-related deaths, driven by its invasive and metastatic nature. Circular RNAs (circRNAs) are increasingly recognized as regulators of cancer progression, primarily through miRNA sponging and interactions with RNA-binding proteins. Their dysregulation has been linked to the development of in various cancers. The present study aimed to investigate the potential involvement of circSLC22A3 in the pathogenesis of ESCC.

methodsCircSLC22A3 expression in ESCC tissues and cells was analyzed using transcriptome sequencing and RT-qPCR. Its circular structure was validated through Sanger sequencing, agarose gel electrophoresis, RNase R digestion, and random priming assays. Subcellular localization was determined by nucleoplasmic separation and fluorescence in situ hybridization (FISH). Clinical correlations were assessed via tissue microarrays. Functional roles of circSLC22A3 in ESCC progression were investigated through in vitro and in vivo assays. Downstream miR-19b-3p and target gene TRAK2 were screened by bioinformatics analysis and RT-qPCR, with binding confirmed via luciferase reporter assays. RNA pulldown combined with RNA immunoprecipitation (RIP) identified IGF2BP1 as a circSLC22A3-interacting protein. RNA-seq and RT-qPCR revealed ACSBG1 as a key downstream effector. IGF2BP1-mediated m

resultsSignificant downregulation of circSLC22A3 was observed in both ESCC tissues and cell lines. Overexpression of circSLC22A3 significantly reduced ESCC cells' migration and invasion capabilities. Mechanistic investigation revealed that circSLC22A3 played a pivotal role in the invasion and metastasis of esophageal cancer through distinct pathways. On one hand, circSLC22A3 functioned as a miR-19b-3p sponge to augment trafficking kinesin protein 2 (TRAK2) expression, while, on the other hand, circSLC22A3 formed a protein-RNA complex with IGF2BP1, resulting in the degradation of acyl-CoA synthetase bubblegum family member 1 (ACSBG1) mRNA through the recognition of m

conclusionsThe present study identified circSLC22A3 as a new tumor suppressor that inhibited ESCC progression through both the circSLC22A3/ miR-19b-3p/ TRAK2 and circSLC22A3/ IGF2BP1/ ACSBG1 axes.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaMicroRNAsRNA-Binding ProteinsRNA, CircularAnimalsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNeoplasm InvasivenessIGF2BP1 protein, humanMicroRNAsMIRN19A microRNA, humanRNA-Binding ProteinsRNA, CircularRNA, MessengerACSBG1circSLC22A3ESCCIGF2BP1miR-19b-3pTRAK2

Identifiers

PMID40448098
PMCPMC12125856

What Socratic holds

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LicenceCC BY
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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 Socratic graph.