ArticleCarcinogenesis2024
Triterpenoid ursolic acid regulates the environmental carcinogen benzo[a]pyrene-driven epigenetic and metabolic alterations in SKH-1 hairless mice for skin cancer interception.
Article in Carcinogenesis, 2024. 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.
- Ursolic acid as a multifunctional anticancer agent with insights into molecular mechanisms therapeutic potential and formulation strategies.Discover oncology · 2026Review
- The Nutrigenomic Effect of Mela Rosa Marchigiana Callus Extract on Cellular Senescence: Insight From a Preliminary In Vitro Study.Molecular nutrition & food research · 2025Article
- Cancer-specific Regulation of Metabolic and Epigenetic Pathways by Dietary Phytochemicals.Pharmaceutical research · 2025Review
- Ursolic Acid as a Protective Agent against UVB-Induced Metabolic and Epigenetic Alterations in Human Skin Keratinocytes: An Omics-Based Study.Cancer prevention research (Philadelphia, Pa.) · 2025Article
- Application of Metabolomics in Carcinogenesis and Cancer Prevention by Dietary Phytochemicals.Current pharmacology reports · 2025Review
- Cyproheptadine inhibits in vitro and in vivo lung metastasis and drives metabolic rewiring.Molecular biology reports · 2024Article
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Authors and funding
13 authors.
Funding
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental carcinogens accountable to developing skin cancers. Recently, we reported that exposure to benzo[a]pyrene (B[a]P), a common PAH, causes epigenetic and metabolic alterations in the initiation, promotion and progression of non-melanoma skin cancer (NMSC). As a follow-up investigation, this study examines how dietary triterpenoid ursolic acid (UA) regulates B[a]P-driven epigenetic and metabolic pathways in SKH-1 hairless mice. Our results show UA intercepts against B[a]P-induced tumorigenesis at different stages of NMSC. Epigenomic cytosines followed by guanine residues (CpG) methyl-seq data showed UA diminished B[a]P-mediated differentially methylated regions (DMRs) profiles. Transcriptomic RNA-seq revealed UA revoked B[a]P-induced differentially expressed genes (DEGs) of skin cancer-related genes, such as leucine-rich repeat LGI family member 2 (Lgi2) and kallikrein-related peptidase 13 (Klk13), indicating UA plays a vital role in B[a]P-mediated gene regulation and its potential consequences in NMSC interception. Association analysis of DEGs and DMRs found that the mRNA expression of KLK13 gene was correlated with the promoter CpG methylation status in the early-stage comparison group, indicating UA could regulate the KLK13 by modulating its promoter methylation at an early stage of NMSC. The metabolomic study showed UA alters B[a]P-regulated cancer-associated metabolisms like thiamin metabolism, ascorbate and aldarate metabolism during the initiation phase; pyruvate, citrate and thiamin metabolism during the promotion phase; and beta-alanine and pathothenate coenzyme A (CoA) biosynthesis during the late progression phase. Taken together, UA reverses B[a]P-driven epigenetic, transcriptomic and metabolic reprogramming, potentially contributing to the overall cancer interception against B[a]P-mediated NMSC.
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