ArticleOncogene2024
Elevated choline drives KLF5-dominated transcriptional reprogramming to facilitate liver cancer progression.
Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Injectable multi-component hydrogel as an inhibitor of choline kinase α achieved the treatment of malignant ascites by inhibiting PI3K/AKT/mTOR signaling pathway.Journal of advanced research · 2026Article
- Advances in Lipid Metabolism Reprogramming in Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2026Review
- Choline metabolism drives metastasis in BRCA1-deficient ovarian cancers by activating FAM3C.Nature communications · 2026Article
- Metabolomics and proteomics analyses reveal the potiental mechanisms underlying colorectal cancer and chemotherapy targets.BMC cancer · 2026Article
- Crosstalk BetweenCancers · 2026Review
- Integrated spatial transcriptome and metabolism study reveals metabolic heterogeneity in human bladder cancer.Cancer gene therapy · 2025Article
- SFP6 fluorescent probes for imaging SAM dynamics in living cells.Mikrochimica acta · 2025Article
- Targeting super-enhancers in liver cancer: from pathogenic mechanisms to clinical applications.Frontiers in pharmacology · 2025Review
- CHML regulates migration and invasion in hepatocellular carcinoma via transcriptional and metabolic reprogramming.Frontiers in oncology · 2025Article
- Dissecting the role of KLF5: from tumor progression to immune interactions with emphasis on glioma and bladder cancer.Frontiers in immunology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
An increase in the total choline-containing compound content is a common characteristic of cancer cells, and aberrant choline metabolism in cancer is closely associated with malignant progression. However, the potential role of choline-induced global transcriptional changes in cancer cells remains unclear. In this study, we reveal that an elevated choline content facilitates hepatocellular carcinoma (HCC) cell proliferation by reprogramming Krüppel-like factor 5 (KLF5)-dominated core transcriptional regulatory circuitry (CRC). Mechanistically, choline administration leads to elevated S-adenosylmethionine (SAM) levels, inducing the formation of H3K4me1 within the super-enhancer (SE) region of KLF5 and activating its transcription. KLF5, as a key transcription factor (TF) of CRC established by choline, further transactivates downstream genes to facilitate HCC cell cycle progression. Additionally, KLF5 can increase the expression of choline kinase-α (CHKA) and CTP:phosphocholine cytidylyltransferase (CCT) resulting in a positive feedback loop to promote HCC cell proliferation. Notably, the histone deacetylase inhibitor (HDACi) vorinostat (SAHA) significantly suppressed KLF5 expression and liver tumor growth in mice, leading to a prolonged lifespan. In conclusion, these findings highlight the epigenetic regulatory mechanism of the SE-driven key regulatory factor KLF5 conducted by choline metabolism in HCC and suggest a potential therapeutic strategy for HCC patients with high choline content.
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