Evidence map›Paper›PMID 40781225›Full record

ArticleCell death & disease2025

SPAT inhibits LUAD metastasis by targeting SF1-mediated splicing.

Yun Ma, Xiaoxu Zhou, Mengqian Yu, Xiang Cheng, Juze Yang, Jiayi Ren, Chengcai Zheng, Jia Li, Xinyi Qian, Jiani Yi and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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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.

Yun Ma *Department of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xiaoxu Zhou *Zhejiang Provincial Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Mengqian Yu *Zhejiang Provincial Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xiang Cheng *Zhejiang Provincial Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Juze YangDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jiayi RenDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Chengcai ZhengZhejiang Provincial Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jia LiDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xinyi QianDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jiani YiDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Honghe ZhangDepartment of Pathology, Research Unit of Intelligence Classification of Tumor Pathology and Precision Therapy, Chinese Academy of Medical Sciences, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.ORCID http://orcid.org/0000-0001-5954-2857
Yan LuZhejiang Provincial Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. yanlu76@zju.edu.cn.ORCID http://orcid.org/0000-0002-5004-4656
Pengyuan LiuDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. pyliu@zju.edu.cn.ORCID http://orcid.org/0000-0002-8386-8416

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) progression involves alterations in oncogenes and tumor suppressor genes, collectively shaping tumorigenic landscape. However, the precise interactions within this landscape remain inadequately understood. Here, we present a functional characterization of a novel long non-coding RNA (lncRNA), SPAT (splice associated transcript). SPAT is downregulated in LUAD and its expression positively correlates with favorable prognosis. In vitro and in vivo experiments demonstrated that SPAT inhibits the migration of LUAD cells. This inhibitory effect is mediated by SPAT's interaction with splicing factor 1 (SF1), which disrupts SF1-mediated splicing of KITLG/SCF exon 6, thereby suppressing ERK phosphorylation. Our findings suggest that SPAT acts as a tumor suppressor in LUAD by regulating alternative splicing and highlight its potential as a therapeutic target for managing LUAD metastasis. SPAT suppresses LUAD cell migration by binding to splicing factor 1 (SF1) and disrupting SF1-mediated inclusion of exon 6 in the KITLG/SCF transcript. This shifts KITLG splicing toward increased production of KITLG-201 isoform and reduced KITLG-205, ultimately lowering ERK phosphorylation and limiting metastatic potential.

Indexed as

Adenocarcinoma of LungLung NeoplasmsRNA, Long NoncodingRNA Splicing FactorsAlternative SplicingAnimalsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNeoplasm MetastasisPhosphorylationRNA, Long NoncodingRNA Splicing FactorsSF1 protein, human

Identifiers

PMID40781225
PMCPMC12334704

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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.