ArticleCancer gene therapy2023
Exploration of a screening model for intrahepatic cholangiocarcinoma patients prone to cuproptosis and mechanisms of the susceptibility of CD274-knockdown intrahepatic cholangiocarcinoma cells to cuproptosis.
Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Tudor domain-containing protein 9-targeting siRNA nanoparticles alleviate Pseudomonas aeruginosa lung injury in preclinical models by promoting neutrophil cuproptosis.Nature communications · 2026Article
- Metal homeostasis as a therapeutic lever: advancing metalloimmunology to remodel the tumor microenvironment and enhance cancer immunotherapy.Theranostics · 2026Review
- Targeting cuproptosis in liver cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2025Review
- Assessing the prognostic and therapeutic value of cuproptosis-related genes in colon adenocarcinoma patients.Frontiers in cell and developmental biology · 2025Article
- Copper homeostasis and copper-induced cell death in tumor immunity: implications for therapeutic strategies in cancer immunotherapy.Biomarker research · 2024Review
- Targeting cuproplasia and cuproptosis in cancer.Nature reviews. Clinical oncology · 2024Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrahepatic cholangiocarcinoma (ICC) is a form of liver cancer with poor long-term survival rates that requires novel therapeutic methods. Our team's previous research found that ICC patients prone to cuproptosis possessed a more satisfactory long-term prognosis and a more sensitive response to copper carrier Elesclomol. Thus, we aimed to identify new diagnostic and treatment strategies for ICC patients prone to cuproptosis and further explore the associated intracellular and extracellular mechanisms of ICC cells prone to cuproptosis. We employed FU-ICC (n = 255) as the training dataset, and validated our findings using SRRSH-ICC (from our center, n = 65), GSE26566 (n = 104), E-MTAB-6389 (n = 78), and scRNA-seq (n = 14) datasets. Single sample gene set enrichment analysis and subsequent unsupervised cluster analysis was conducted on the training dataset for the pan-programmed cell death gene set (including apoptosis, autophagy, ferroptosis, pyroptosis, necroptosis, and cuproptosis) to define and screen ICC patients prone to cuproptosis. We constructed a nomogram model using weighted gene co-expression network analysis and machine learning algorithms to predict ICC patients prone to cuproptosis, then explored its clinical value with multi-center transcriptome profiling. Furthermore, we validated the hub genes with in vitro and animal experiments to define ICC cells prone to cuproptosis. Ultimately, bulk and single-cell transcriptome profiling were utilized to explore the immune microenvironment of ICC cells prone to cuproptosis. Our nomogram model could help predict ICC patients prone to cuproptosis and possessed excellent prediction efficiency and clinical significance via internal and external verification. In vitro experiments demonstrated that ICC cells with siRNA-mediated knockdown of CD274 (PD-L1) and stimulation with elescomol-CuCl
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