ArticleOncology reports2018
Emodin induces apoptosis in human hepatocellular carcinoma HepaRG cells via the mitochondrial caspase‑dependent pathway.
Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Potential Hepatotoxins Found in Herbal Medicinal Products: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Emodin and the Anthraquinone Scaffold: Therapeutic Promise and Strategies to Overcome Translational Barriers.Molecules (Basel, Switzerland) · 2026Review
- Comprehensive Review on the Toxicity of Five Main AQ Constituents from Rhubarb: Mechanisms, Challenges and Future Perspectives.Drug design, development and therapy · 2026Review
- Current status and trend of global research on the pharmacological effects of emodin family: bibliometric study and visual analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Mechanism of microRNA-124-3p targeting calpain-1 to affect the function of intervertebral disc nucleus pulposus cells.Cytotechnology · 2025Article
- Evaluating anticancer activity of emodin by enhancing antioxidant activities and affecting PKC/ADAMTS4 pathway in thioacetamide-induced hepatocellular carcinoma in rats.Redox report : communications in free radical research · 2024Article
- Natural Products and Altered Metabolism in Cancer: Therapeutic Targets and Mechanisms of Action.International journal of molecular sciences · 2024Review
- Review
- Isoliquiritigenin as a modulator of the Nrf2 signaling pathway: potential therapeutic implications.Frontiers in pharmacology · 2024Review
- Emodin is a Potential Drug Targeting CD44-positive Hepatocellular Cancer.Current cancer drug targets · 2024Article
- Structural Characterization and Anticancer Activity of a New Anthraquinone fromPharmaceuticals (Basel, Switzerland) · 2023Article
- The In Vitro Anti-Parasitic Activities of Emodin towardPharmaceuticals (Basel, Switzerland) · 2023Article
- Emodin Sensitizes Cervical Cancer Cells to Vinblastine by Inducing Apoptosis and Mitotic Death.International journal of molecular sciences · 2022Article
- Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin.BMC cancer · 2022Article
- Bruceine D Identified as a Drug Candidate against Breast Cancer by a Novel Drug Selection Pipeline and Cell Viability Assay.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers.International journal of biological sciences · 2022Review
- Idiosyncratic liver injury induced by bolus combination treatment with emodin and 2,3,5,4'-tetrahydroxystilbene-2-Frontiers in pharmacology · 2022Article
- Molecular mechanisms and associated cell signalling pathways underlying the anticancer properties of phytochemical compounds fromExperimental and therapeutic medicine · 2021Review
- Long non-coding RNA RP11-81H3.2 suppresses apoptosis by targeting microRNA-1539/COL2A1 in human nucleus pulposus cells.Experimental and therapeutic medicine · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emodin‑induced hepatotoxicity in vivo and in vitro has been gaining increasing attention. However, the exact molecular pathways underlying these effects remain poorly clarified. The aim of the present study was to evaluate the cytotoxic effect of emodin on HepaRG cells and to define the underlying mechanism. The results demonstrated that emodin evidently inhibited HepaRG cell growth in a dose‑ and time‑dependent manner by blocking cell cycle progression in the S and G2/M phase and by inducing apoptosis. Emodin treatment also resulted in generation of reactive oxygen species (ROS), which abrogated mitochondrial membrane potential (MMP). The above effects were all suppressed by antioxidants, such as N‑acetylcysteine (NAC). Further studies by western blot analysis howed that emodin upregulated p53, p21, Bax, cyclin E, cleaved caspase‑3, 8 and 9, and cleaved poly(ADP‑ribose)polymerase (PARP). However, the protein expression of Bcl‑2, cyclin A and CDK2 was downregulated. Taken together, our results suggest that emodin induces apoptosis via the mitochondrial apoptosis pathway through cell cycle arrest and ROS generation in HepaRG cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.