ArticleCancer science2024
Itraconazole inhibits tumor growth via CEBPB-mediated glycolysis in colorectal cancer.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Repurposing Non-oncologic Drugs via Targeted Nanocarriers for Cancer Therapy: Mechanisms, Synergistic Combinations, and Clinical Translation.AAPS PharmSciTech · 2026Review
- Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights.RSC advances · 2026Review
- TCF7L2/DEPDC1 axis contributes to tumor progression by promoting cell proliferation, aerobic glycolysis, and immunosuppression in pancreatic cancer.Clinical and experimental medicine · 2026Article
- DCUN1D5 promotes the proliferation and migration of colorectal cancer tumors in vitro and in vivo.Cancer cell international · 2026Article
- Repurposing Itraconazole in Combination with Chemotherapy and Immune Checkpoint Inhibitor for Cancer.Medical sciences (Basel, Switzerland) · 2026Review
- Cholesterol metabolism and cancer: Molecular mechanisms, immune regulation and an epidemiological perspective (Review).International journal of molecular medicine · 2025Review
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- Phytochemical profiling and anticancer potential of pistachio wastes against MCF-7 breast cancer cells: a metabolic and apoptotic pathway analysis.BMC complementary medicine and therapies · 2025Article
- Vitamin D3 augments cytotoxic effect of Itraconazole on chronic myelogenous leukemia cell line: a synergic effect on AMPK/AKT signaling pathway.Molecular biology reports · 2025Article
- The highly expressedJournal of gastrointestinal oncology · 2025Article
- The Role of Key Glycolytic Enzymes in the Diagnosis, Treatment, and Immune Microenvironment of Colorectal Cancer.Human mutation · 2025Review
- Integrated transcriptomic analysis reveals a CEBPB-DUSP1 axis driving tumor progression in colorectal cancer.PloS one · 2025Article
- Article
- DPEP Inhibits Cancer Cell Glucose Uptake, Glycolysis and Survival by Upregulating Tumor Suppressor TXNIP.Cells · 2024Article
- Itraconazole inhibits tumor growth via CEBPB-mediated glycolysis in colorectal cancer.Cancer science · 2024Article
- Knockdown of Stanniocalcin-1 inhibits growth and glycolysis in oral squamous cell carcinoma cells.Open life sciences · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Advanced colorectal cancer (CRC) is characterized by a high recurrence and metastasis rate, which is the primary cause of patient mortality. Unfortunately, effective anti-cancer drugs for CRC are still lacking in clinical practice. We screened FDA-approved drugs by utilizing targeted organoid sequencing data and found that the antifungal drug itraconazole had a potential therapeutic effect on CRC tumors. However, the effect and mechanism of itraconazole on CRC tumors have not been investigated. A cell line-derived xenograft model in tumor-bearing mice was established and single-cell RNA sequencing was performed on tumor samples from four mice with or without itraconazole treatment. The proportion of cell populations and gene expression profiles was significantly different between the two groups. We found that itraconazole could inhibit tumor growth and glycolysis. We revealed that CEBPB was a new target for itraconazole, and that silencing CEBPB could repress CRC glycolysis and tumor growth by inhibiting ENO1 expression. Clinical analysis showed that CEBPB expression was obviously elevated in CRC patients, and was associated with poor survival. In summary, itraconazole treatment remodeled cell composition and gene expression profiles. Itraconazole inhibited cell glycolysis and tumor growth via the CEBPB-ENO1 axis. In this study, we illustrate a new energy metabolism mechanism for itraconazole on tumor growth in CRC that will provide a theoretical basis for CRC targeting/combination therapy.
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Registered trials
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.