Evidence map›Paper›PMID 39840666›Full record

ArticleThoracic cancer2025

miR-224-5p Suppresses Non-Small Cell Lung Cancer via IL6ST-Mediated Regulation of the JAK2/STAT3 Pathway.

Jiao Tian, Yiming He, Zihui Zhang, Yuxin Zhu, Haixia Ren, Liang Zhang, Lei Li, Wei Li, Weidong Zhang, Ting Xiao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thoracic cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
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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

12 authors.

Jiao TianDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Yiming HeDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Zihui ZhangDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Yuxin ZhuDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Haixia RenDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Liang ZhangDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Lei LiDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Wei LiDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Weidong ZhangDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Ting XiaoDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Honggang ZhouDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.ORCID https://orcid.org/0000-0003-2987-3422
Xiaoping LiDepartment of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.ORCID https://orcid.org/0000-0001-6549-8709

Funding

Foundation of Organ Fibrosis Drug Gability Joint Research Centre of Nankai and Guokaixingcheng 735-F1040051Tianjin Science and Technology Project 20JCYBJC00600
6 · The paper itself

Abstract

backgroundOur study aimed to explore the specific functions and potential mechanisms of miR-224-5p in non-small cell lung cancer (NSCLC).

methodsWe first analyzed the expression of miR-224-5p in NSCLC patients and cell lines through the GEO database and qRT-PCR analysis. Then, we used MTT assays, wound healing assays, Transwell assays, and western blotting to evaluate the effects of miR-224-5p on NSCLC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Furthermore, we used a xenograft tumor model to evaluate the effect of miR-224-5p on NSCLC tumor growth. Potential binding targets of miR-224-5p were further identified through the target prediction databases, and the relationships between miR-224-5p, its targets, and downstream signaling pathways were further verified using luciferase reporter gene assays and western blotting.

resultsThe GEO database and qRT-PCR analysis indicated that miR-224-5p was significantly downregulated in NSCLC patients and cell lines. Functional assays indicated that inhibiting miR-224-5p could enhance the proliferation, migration, invasion, and EMT of NSCLC cells, as well as accelerate tumor growth. In contrast, overexpression of miR-224-5p inhibited these processes. We identified IL6ST (interleukin 6 signal transducer) as a binding target of miR-224-5p. We observed that miR-224-5p could bind to and inhibit IL6ST expression and JAK2/STAT3 signaling pathway, and the inhibition of NSCLC tumor growth and JAK2/STAT3 pathway by miR-224-5p could be reversed by IL6ST overexpression.

conclusionOur study demonstrated that miR-224-5p inhibited NSCLC by targeting IL6ST, thereby downregulating the JAK2/STAT3 signaling pathway.

Indexed as

Carcinoma, Non-Small-Cell LungJanus Kinase 2Lung NeoplasmsMicroRNAsSTAT3 Transcription FactorAnimalsCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeSignal TransductionJAK2 protein, humanJanus Kinase 2MicroRNAsSTAT3 protein, humanSTAT3 Transcription FactorIL6STJAK2/STAT3 signaling pathwaymiR‐224‐5pNSCLC

Identifiers

PMID39840666
PMCPMC11751714

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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.