ArticleJournal of experimental & clinical cancer research : CR2018
C-Myc-dependent repression of two oncogenic miRNA clusters contributes to triptolide-induced cell death in hepatocellular carcinoma cells.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Triptolide as a multi-target anticancer agent: molecular mechanisms and translational potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Research progress on active components from natural medicines inhibiting tumor via epigenetic regulation.Molecular biology reports · 2026Review
- miR-17: from developmental regulatory hub to molecular engine driving tumourigenesis.Frontiers in oncology · 2026Review
- Co‑treatment with triptolide and RSL3 induces hepatocellular carcinoma cell apoptosis and ferroptosis.Molecular medicine reports · 2025Article
- Cytohesin-4/ARF6 facilitates the progression of acute myeloid leukemia through activating PIK3R5/PI3K/AKT pathway.iScience · 2025Article
- Pharmacological, computational, and mechanistic insights into triptolide's role in targeting drug-resistant cancers.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- PDCD11 Stabilizes C-MYC Oncoprotein by Hindering C-MYC-SKP2 Negative Feedback Loop to Facilitate Progression of p53-Mutant Breast and Colon Malignancies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions.MedComm · 2025Review
- Research Progress on Natural Products That Regulate miRNAs in the Treatment of Osteosarcoma.Biology · 2025Review
- Histone Methyltransferase SETD1B Maintains Cancer Stem Cell Niche by Regulating the Crosstalk between CD24 and Surface Adhesion Molecules in Hepatocellular Carcinoma.International journal of biological sciences · 2025Article
- Functions and targets of miRNAs in pharmacological and toxicological effects of major components of Tripterygium wilfordii Hook F.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Article
- Self-Amplified pH/ROS Dual-Responsive Co-Delivery Nano-System with Chemo-Photodynamic Combination Therapy in Hepatic Carcinoma Treatment.International journal of nanomedicine · 2024Article
- The role of microRNAs in hepatocellular carcinoma: Therapeutic targeting of tumor suppressor and oncogenic genes.Clinical and experimental hepatology · 2023Review
- Irf7 regulates the expression of Srg3 and ferroptosis axis aggravated sepsis-induced acute lung injury.Cellular & molecular biology letters · 2023Article
- γ-Cyclodextrin metal-organic framework as a carrier to deliver triptolide for the treatment of hepatocellular carcinoma.Drug delivery and translational research · 2022Article
- Elucidating miRNA Function in Cancer Biology via the Molecular Genetics' Toolbox.Biomedicines · 2022Review
- OMICS Applications for Medicinal Plants in Gastrointestinal Cancers: Current Advancements and Future Perspectives.Frontiers in pharmacology · 2022Review
- MicroRNAs as crucial mediators in the pharmacological activities of triptolide (Review).Experimental and therapeutic medicine · 2021Review
- c-Myc Upregulated by High Glucose Inhibits HaCaT Differentiation by S100A6 Transcriptional Activation.Frontiers in endocrinology · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundTriptolide is a structurally unique diterpene triepoxide with potent antitumor activity. However,the effect and mechanism of triptolide on hepatocellular carcinoma (HCC) is not well studied.
methodsCells were treated with triptolide, and the anti-HCC activity of triptolide was evaluated using flow cytometry, western blot, and xenograft studies. MicroRNA microarray and quantitative reverse-transcription polymerase chain reaction was used to identify differential microRNAs induced by triptolide. Chromatin immunoprecipitation assay was employed to study the interaction between c-Myc and genomic regions of miR106b-25. MicroRNAs overexpression and knockdown experiments were performed to determine the role of these microRNAs in triptolide-induced apoptosis.
resultsTriptolide inhibited cell proliferation and induced marked apoptosis in multiple HCC cell lines with different p53 status. Several signaling molecules involved in different pathways were altered after the treatment of triptolide. Xenograft tumor volume was significantly reduced in triptolide-treated group compared with vehicle control group. Two miRNA clusters, miR-17-92 and miR-106b-25, were significantly suppressed by triptolide, which resulted in the upregulation of their common target genes, including BIM, PTEN, and p21. In HCC samples, high levels of these miRNA clusters correlated with shorter recurrence free survival. Triptolide inhibited the expression of theses miRNAs in a c-Myc-dependent manner, which enhanced triptolide-induced cell death. We further showed that triptolide down-regulated the expression of c-Myc through targeting ERCC3, a newly identified triptolide-binding protein.
conclusionsThe triptolide-induced modulation of c-Myc/miRNA clusters/target genes axis enhances its potent antitumor activity, which indicates that triptolide serves as an attractive chemotherapeutic agent against HCC.
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Registered trials
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