ArticleBMC cancer2022
Tryptophan hydroxylase 1 drives glioma progression by modulating the serotonin/L1CAM/NF-κB signaling pathway.
Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 22 citations in OpenAlex.
- Theacrine-rich Jianghua Kucha black tea alleviates depressionRSC advances · 2026Article
- Neuro-immune crosstalk in the tumor microenvironment: mechanisms and therapeutic implications for cancer immunotherapy.Journal of neuroinflammation · 2026Review
- The molecular footprint of the serotoninergic system in human glioblastoma cells.Journal of molecular histology · 2025Article
- Proteomic profiling reveals dynamic regulation of vesicle trafficking across glioma grades.Journal of neuro-oncology · 2025Article
- Review
- Identifying survival subtypes with autoencoder using multiple types of high-dimensional genomic data from studies of glioblastoma multiforme.Briefings in bioinformatics · 2025Article
- Gut microbiota and their influence in brain cancer milieu.Journal of neuroinflammation · 2025Review
- Amino acid metabolism in glioblastoma pathogenesis, immune evasion, and treatment resistance.Cancer cell international · 2025Review
- The Prognostic Significance of TMSB4X in Glioma Patients.International journal of general medicine · 2025Article
- Molecular mechanisms and therapeutic significance of Tryptophan Metabolism and signaling in cancer.Molecular cancer · 2024Review
- Navigating glioblastoma complexity: the interplay of neurotransmitters and chromatin.Molecular biology reports · 2024Review
- Role of Serotonergic System in Regulating Brain Tumor-Associated Neuroinflammatory Responses.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The Recent Research Progress of NF-κB Signaling on the Proliferation, Migration, Invasion, Immune Escape and Drug Resistance of Glioblastoma.International journal of molecular sciences · 2023Review
- Gut microbiota mediated the individualized efficacy of Temozolomide via immunomodulation in glioma.Journal of translational medicine · 2023Article
- Trends in metabolic signaling pathways of tumor drug resistance: A scientometric analysis.Frontiers in oncology · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioma is one of the main causes of cancer-related mortality worldwide and is associated with high heterogeneity. However, the key players determining the fate of glioma remain obscure. In the present study, we shed light on tumor metabolism and aimed to investigate the role of tryptophan hydroxylase 1 (TPH-1) in the advancement of glioma.
methodHerein, the levels of TPH-1 expression in glioma tissues were evaluated using The Cancer Genome Atlas (TCGA) database. Further, the proliferative characteristics and migration ability of TPH-1 overexpressing LN229/T98G cells were evaluated. Additionally, we performed a cytotoxicity analysis using temozolomide (TMZ) in these cells. We also examined the tumor growth and survival time in a mouse model of glioma treated with chemotherapeutic agents and a TPH-1 inhibitor.
resultsThe results of both clinical and experimental data showed that excess TPH-1 expression resulted in sustained glioma progression and a dismal overall survival in these patients. Mechanistically, TPH-1 increased the production of serotonin in glioma cells. The elevated serotonin levels then augmented the NF-κB signaling pathway through the upregulation of the L1-cell adhesion molecule (L1CAM), thereby contributing to cellular proliferation, invasive migration, and drug resistance. In vivo experiments demonstrated potent antitumor effects, which benefited further from the synergistic combination of TMZ and LX-1031.
conclusionTaken together, these data suggested that TPH-1 facilitated cellular proliferation, migration, and chemoresistance in glioma through the serotonin/L1CAM/NF-κB pathway. By demonstrating the link of amino acid metabolic enzymes with tumor development, our findings may provide a potentially viable target for therapeutic manipulation aimed at eradicating glioma.
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