ArticleInternational journal of molecular sciences2018
Emodin Sensitizes Hepatocellular Carcinoma Cells to the Anti-Cancer Effect of Sorafenib through Suppression of Cholesterol Metabolism.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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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
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Pooled it
- Revisiting cholesterol metabolism in hepatocellular carcinoma: a hidden driver of systemic therapy response.ESMO gastrointestinal oncology · 2026Review
- Metabolic reprogramming-driven resistance to multi-kinase inhibitors in hepatocellular carcinoma: molecular mechanisms and therapeutic opportunities.Molecular cancer · 2026Review
- Synergistic Interactions of Anthraquinones with Conventional Cancer Therapies.Combinatorial chemistry & high throughput screening · 2026Review
- Research Progress on Quinone Compounds for the Treatment of Hepatocellular Carcinoma.Biomolecules · 2025Review
- Targeting cholesterol metabolism: a promising therapy strategy for cancer.Acta pharmacologica Sinica · 2025Review
- Unlocking the lipid code: SREBPs as key drivers in gastrointestinal tumour metabolism.Lipids in health and disease · 2025Review
- Modulating the JAK/STAT pathway with natural products: potential and challenges in cancer therapy.Discover oncology · 2025Review
- Role of emodin to prevent gastrointestinal cancers: recent trends and future prospective.Discover oncology · 2025Review
- The Role of Cholesterol Metabolism and Its Regulation in Tumor Development.Cancer medicine · 2025Review
- Shikonin a potent phytotherapeutic: a comprehensive review on metabolic reprogramming to overcome drug resistance in cancer.Molecular biology reports · 2025Review
- Emodin reverses sorafenib resistance in hepatocellular carcinoma by inhibiting epithelial-mesenchymal transition via the Akt signaling pathway.Translational cancer research · 2025Article
- Targeting lipid reprogramming in the tumor microenvironment by traditional Chinese medicines as a potential cancer treatment.Heliyon · 2024Review
- Drug repurposing for cancer therapy.Signal transduction and targeted therapy · 2024Review
- A Novel Combinatorial Regimen Using Sorafenib and Uttroside B, A US FDA-designated 'Orphan Drug', for the Treatment of Hepatocellular Carcinoma.Anti-cancer agents in medicinal chemistry · 2024Article
- Research Progress on the Anti-Liver Cancer Mechanism and Toxicity of Rhubarb Anthraquinone.Drug design, development and therapy · 2024Review
- SREBP Regulation of Lipid Metabolism in Liver Disease, and Therapeutic Strategies.Biomedicines · 2023Review
- A mannitol-modified emodin nano-drug restores the intestinal barrier function and alleviates inflammation in a mouse model of DSS-induced ulcerative colitis.Chinese medicine · 2023Article
- SREBP2 inhibitor betulin sensitizes hepatocellular carcinoma to lenvatinib by inhibiting the mTOR/IL-1β pathway.Acta biochimica et biophysica Sinica · 2023Article
- Lipid metabolism of hepatocellular carcinoma impacts targeted therapy and immunotherapy.World journal of gastrointestinal oncology · 2023Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reduced therapeutic efficacy of sorafenib, a first-generation multikinase inhibitor, is often observed during the treatment of advanced hepatocellular carcinoma (HCC). Emodin is an active component of Chinese herbs, and is effective against leukemia, lung cancer, colon cancer, pancreatic cancer, and HCC; however, the sensitizing effect of emodin on sorafenib-based HCC therapy has not been evaluated. Here, we demonstrate that emodin significantly improved the anti-cancer effect of sorafenib in HCC cells, such as HepG2, Hep3B, Huh7, SK-HEP-1, and PLC/PRF5. Mechanistically, emodin inhibits sterol regulatory element-binding protein-2 (SREBP-2) transcriptional activity, which suppresses cholesterol biosynthesis and oncogenic protein kinase B (AKT) signaling. Additionally, attenuated cholesterol synthesis and oncogenic AKT signaling inactivated signal transducer and activator of transcription 3 (STAT3), an oncogenic transcription factor. Furthermore, emodin synergistically increased cell cycle arrest in the G1 phase and apoptotic cells in the presence of sorafenib. Animal models xenografted with HepG2 or SK-HEP-1 cells also showed that the combination of emodin and sorafenib was sufficient to inhibit tumor growth. Overall, these results suggested that the combination of emodin and sorafenib may offer a potential therapy for patients with advanced HCC.
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