Evidence map›Paper›PMID 40123000›Full record

ArticleCancer gene therapy2025

TOM1L1 mediated the sort of tumor suppressive miR-378a-3p into exosomes and the excretion out of cells to promote ESCC progression.

Lu Wang, Huijuan Liu, Guohui Chen, Qinglu Wu, Songrui Xu, Qichao Zhou, Yadong Zhao, Qiaorong Wang, Ting Yan, Xiaolong Cheng

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Article in Cancer gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Review
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.

Lu WangKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Huijuan LiuKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Guohui ChenKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Qinglu WuKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Songrui XuKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Qichao ZhouKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Yadong ZhaoKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Qiaorong WangKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.
Ting YanKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China. enntei@hotmail.com.
Xiaolong ChengKey Laboratory of Cellular Physiology of the Ministry of Education & Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China. chengxl@sxmu.edu.cn.ORCID http://orcid.org/0000-0001-8726-5631

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes mediate cell-to-cell communication by releasing miRNAs, mRNA, etc. However, there is little research about the effects on the donor cells after miRNAs are excreted out of cells through exosomes. Here, we found that miR-378a-3p was specifically enriched in exosomes and inhibited cell proliferation, migration, invasion, and colony formation in ESCC. In addition, miR-378a-3p was sorted into exosomes through TOM1L1 and extracted mainly out of ESCC cells. Overexpression of TOM1L1 led to tumor suppressor miR-378a-3p accumulation in exosomes rather than in donor cells, promoting ESCC progression. Moreover, miR-378a-3p targets DYRK1A that directly binds to NPM1 and the phosphorylation state of NPM1 at Ser125 to suppress tumor growth. Taken together, our findings demonstrate that TOM1L1-mediated the tumor suppressor miR-378a-3p into exosomes and excreted out of cells to promote tumor progression.

Indexed as

Esophageal NeoplasmsExosomesMicroRNAsAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceMice, NudeNucleophosminProtein Serine-Threonine KinasesMicroRNAsMIRN378 microRNA, humanNPM1 protein, humanNucleophosminProtein Serine-Threonine Kinases

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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.