Evidence map›Paper›PMID 41916911›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2026

[Expression, Prognostic and Functional Analysis of SRSF Family Proteins 
in Non-small Cell Lung Cancer].

Shuqi Tu, Yuhao Chen, Yalong Zhang, Qiang Chen, Yaguang Fan, Yixuan Wang, Yang Zhang, Sinuo Li, Jun Chen, Hongli Pan and 2 more

Abstract readEnglish Abstract
In one paragraph

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Shuqi TuTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Yuhao ChenTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Yalong ZhangDepartment of Pathology, Binzhou Medical University Hospital, Binzhou 256600, China.
Qiang ChenTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Yaguang FanTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Yixuan WangTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Yang ZhangTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Sinuo LiTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Jun ChenTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Hongli PanTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Xuexia ZhouTianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Xuebing LiTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths worldwide, and its occurrence and development are closely related to complex molecular mechanisms. Alternative splicing of precursor mRNA is a key step in gene expression regulation, and its dysregulation is common in tumors. The serine/arginine-rich splicing factor (SRSF) family, a core protein family in splicing regulation, has been confirmed to play oncogenic roles in various cancers. However, systematic research on the SRSF family in NSCLC remains insufficient. This study aims to systematically analyze the specific expression patterns, clinical prognostic value, collaborative mechanisms and potential biological functions of SRSF individual members in NSCLC by the combination of bioinformatics analysis and experimental verification.

methodsThis study integrated NSCLC transcriptome data and clinical information from public databases such as The Cancer Genome Atlas (TCGA) and the Cancer Cell Line Encyclopedia (CCLE), and systematically analyzed the differential expressions of SRSF family members. Kaplan-Meier survival analysis was performed to assess the correlation between the expression levels of each SRSF member and patients' overall survival (OS). Furthermore, co-expression network analysis and Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were employed to explore the biological processes and signaling pathways potentially involved by the SRSF family. Moreover, the expression and function of key members were verified by reverse transcription quantitative polymerase chain reaction (RT-qPCR), cell counting kit-8 (CCK-8) and cell proliferation experiments in clinical samples and cell lines.

resultsMultiple members of the SRSF family (e.g., SRSF1, SRSF2, SRSF3, SRSF6, SRSF7, SRSF9, SRSF10) were found to be significantly upregulated in NSCLC tissues and cell lines. Survival analysis indicated that high expression of SRSF9 was associated with poor prognosis, while low expressions of SRSF11 and SRSF12 also indicated unfavorable outcomes. Functional enrichment analysis revealed that the SRSF family is not only involved in RNA splicing but also significantly enriched in pathways related to protein homeostasis, cellular stress response, and neurodegenerative diseases. In vitro experiments confirmed that knockdown of SRSF1, SRSF2, SRSF6, SRSF9 and SRSF10 significantly inhibited the proliferation of NSCLC cells.

conclusionsThis study systematically delineates the expression and functional landscape of the SRSF family in NSCLC, confirming their potential as prognostic biomarkers and therapeutic targets. The findings suggest that the SRSF family may drive NSCLC progression by disrupting cellular homeostasis, a crucial aspect of tumorigenesis, such as protein homeostasis and stress responses. This research provides a theoretical foundation for a deeper understanding of the role of splicing dysregulation in lung cancer and for the development of novel therapeutic strategies.

Indexed as

Carcinoma, Non-Small-Cell LungGene Expression Regulation, NeoplasticLung NeoplasmsSerine-Arginine Splicing FactorsCell Line, TumorCell ProliferationHumansPrognosisSerine-Arginine Splicing FactorsAlternative splicingBioinformatics analysisCell proliferation and viabilityLung neoplasmsSRSF familySurvival prognosis

Identifiers

PMID41916911
PMCPMC13046443

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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.