ArticleJournal of Cancer2024
Exploring SLC16A1 as an Oncogenic Regulator and Therapeutic Target in Cholangiocarcinoma.
Article in Journal of Cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- tLyP-1 peptide-modified MnO₂ co-delivering si-SLC16A1 and temozolomide synergistically suppresses glioblastoma via hypoxia modulation and metabolic stress.Journal of nanobiotechnology · 2026Article
- Article
- Tumor gene expression signatures associated with outcome in large B-cell lymphoma treated with CD19-directed CAR T-cell therapy (axicabtagene ciloleucel).Frontiers in oncology · 2025Article
- SLC16A1 Inhibits Ferroptosis and Promotes the Progression of Head and Neck Squamous Cell Carcinoma.Journal of Cancer · 2025Article
- Identification of key ferroptosis-related genes and therapeutic target in nasopharyngeal carcinoma.Frontiers in genetics · 2025Article
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Authors and funding
5 authors.
Funding
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Abstract
Cholangiocarcinoma (CCA) is a primary malignant tumor of the liver, typically diagnosed in advanced stages. Surgical resection remains the principal treatment method in clinical practice. Regrettably, the majority of patients receive their diagnosis at an advanced stage, making surgical intervention unfeasible. While chemotherapy serves as the main palliative treatment for advanced CCA, its effectiveness is significantly limited due to the rapid development of chemoresistance. Studying the pathogenesis of CCA and new resistance targets is crucial for improving clinical outcomes. In our current study, we first identified the expression of SLC16A1 in the transcriptome and proteome of human tumors and found abnormal expression of SLC16A1 in various human cancers. Subsequently, we focused our attention on the role of SLC16A1 in CCA. Utilizing bioinformatics analysis, we pioneered the identification of the clinical significance of SLC16A1 in this type of cancer. Specifically, higher expression levels of SLC16A1 were observed in CCA patients with venous invasion and higher T and M stages. Additionally, patients with higher SLC16A1 expression had poorer prognoses. These results suggest the oncogenic role of SLC16A1 in CCA. Further immune infiltration analysis revealed a significant correlation between SLC16A1 and the infiltration levels of cells like neutrophils and macrophages in the tumor microenvironment, indicating SLC16A1's potential involvement in regulating the tumor immune microenvironment of CCA. Moreover, results from functional and pathway enrichment analyses revealed that SLC16A1 might affect clinical outcomes in CCA patients by participating in drug metabolism processes. Finally, through further
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