ArticleMolecular biomedicine2025
5-Hydroxytryptamine promotes non-small cell lung cancer metastasis via the SNRPG/WT1/CDK14 Axis.
Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Cyclins and Cyclin-Dependent Kinases: Structure, Biological Functions, and Innovative Targeting Strategies in Cancer.MedComm · 2026Review
- [Research Progress on the Mechanism of Gut Microbiota Influencing Lung Cancer Brain Metastasis via the Brain-gut Axis].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Tumor metastasis severely compromises the prognosis of patients with non-small cell lung cancer (NSCLC), yet the underlying mechanisms remain unclear. The biogenic amine 5-hydroxytryptamine (5-HT), derived from tryptophan (Trp), has been reported to promote tumor growth, but its role in NSCLC metastasis has not been fully elucitated. In this study, fecal metabolomic profiling revealed significant enrichment of Trp metabolism and serotonergic synapse pathways in patients with NSCLC metastasis. Notably, the levels of 5-HT in peripheral blood showed a positive correlation with fecal Trp concentrations in NSCLC patients. Functional experiments demonstrated that 5-HT promoted NSCLC cell migration, invasion, epithelial-mesenchymal transition (EMT), and metastasis by inhibiting the expression of small nuclear ribonucleoprotein polypeptide G (SNRPG). RNA sequencing (RNA-seq) further identified cyclin-dependent kinase 14 (CDK14) as a critical downstream target of SNRPG. SNRPG downregulated CDK14 expression, thereby restraining malignant phenotypes in NSCLC cells. Furthermore, SNRPG negatively regulated the protein levels of Wilms tumor 1 (WT1) by directly binding to it. Loss of SNRPG led to WT1 accumulation, which in turn bound to the CDK14 promoter and activated transcription, ultimately driving NSCLC metastasis. These findings collectively suggest that the 5-HT/SNRPG/WT1/CDK14 axis plays a pivotal role in promoting NSCLC metastasis and highlight 5-HT and SNRPG as potential therapeutic targets for NSCLC metastasis.
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Registered trials
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