ArticleMolecular therapy oncolytics2022
Berberine inhibits carcinogenesis through antagonizing the ATX-LPA-LPAR2-p38-leptin axis in a mouse hepatoma model.
Article in Molecular therapy oncolytics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Transcriptome and plasma proteome analyses identify susceptibility genes and proteins for alcohol-related hepatocellular carcinoma.Human genomics · 2026Article
- Neg-entropy is the true drug target for chronic diseases.Acta pharmaceutica Sinica. B · 2026Review
- STING Restricts EV-A71 Infection by Regulating T Cell Development and Enhancing Immune Cell Effector Function.International journal of molecular sciences · 2025Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- LPAR6 Participates in Neuropathic Pain by Mediating Astrocyte Cells via ROCK2/NF-κB Signal Pathway.Molecular neurobiology · 2024Article
- The Emerging Role of LPA as an Oncometabolite.Cells · 2024Review
- Cardio-oncology: Shared Genetic, Metabolic, and Pharmacologic Mechanism.Current cardiology reports · 2023Review
- Obesity contributes to hepatocellular carcinoma development via immunosuppressive microenvironment remodeling.Frontiers in immunology · 2023Review
- Study on the molecular mechanism of anti-liver cancer effect of Evodiae fructus by network pharmacology and QSAR model.Frontiers in chemistry · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemoprevention of hepatocellular carcinoma (HCC) is highly desirable in clinic. Berberine (BBR) is reported to play potential roles in cancer treatment and prevention. We studied the chemopreventive effect of BBR on hepatocellular carcinogenesis in an inflammation-driven mouse model, as it was enriched in liver after oral administration. Oral BBR significantly decreased the number and volume of visible nodular tumors, and prolonged the median overall survival by 9 and 8 weeks in the diethylnitrosamine (DEN)-injected male and female mice respectively. The nodular tumors were induced through activation of the lysophosphatidic acid (LPA) pathway in liver. LPA stimulated the abnormal leptin transcription through interacting with LPA receptor-2 (LPAR2) followed by p38 activation, and BBR inhibited carcinogenesis by suppressing the bioactivity of LPA. Specifically, BBR significantly reduced the expression of the LPA synthetase autotaxin (ATX) and LPAR2 in the nodular tumors of DEN-injected mice. Subsequently, BBR repressed the abnormal transcription of leptin stimulated by LPA-induced phosphorylation of p38 in hepatoma cells. In fact, BBR reduced the abnormal expression of leptin in livers of DEN-injected male mice throughout the course of an 8-month experiment. BBR might be a preventive agent for HCC, working at least partially through antagonizing the ATX-LPA-LPAR2-p38-leptin axis in liver.
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