ArticleMolecules (Basel, Switzerland)2022
Acacetin Inhibits Cell Proliferation and Induces Apoptosis in Human Hepatocellular Carcinoma Cell Lines.
Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Role of ZNF652 in Regulating Hepatocellular Carcinoma Cell Proliferation and Apoptosis via the circRHOT1/SLC38A6 Axis.The Kaohsiung journal of medical sciences · 2026Article
- Recent Progress on Polyphenols of Malaysian Honey and Their Molecular Mechanism Pathways in Cancer-A Comprehensive Review.International journal of molecular sciences · 2026Review
- Redox and Bioenergetic Modulation by Acacetin Attenuated Neuropathic Allodynia in Mice with Diet-induced Diabetes.Molecular neurobiology · 2025Article
- Molecular Mechanism Discovery of Acacetin Against Cancers: Insights from Network Pharmacology and Molecular Docking.International journal of molecular sciences · 2025Review
- Mechanistic Insights into the Anticancer Potential of Methoxyflavones Analogs: A Review.Molecules (Basel, Switzerland) · 2025Review
- Acacetin, a Natural Flavone with Potential in Improving Liver Disease Based on Its Anti-Inflammation, Anti-Cancer, Anti-Infection and Other Effects.Molecules (Basel, Switzerland) · 2024Review
- Effect of acacetin on inhibition of apoptosis inWorld journal of gastrointestinal oncology · 2024Article
- Mechanism of acacetin regulating hepatic stellate cell apoptosis based on network pharmacology and experimental verification.Heliyon · 2024Article
- Acacetin exerts antitumor effects on gastric cancer by targeting EGFR.Frontiers in pharmacology · 2023Article
- Effects of Acacetin on the Pharmacokinetics of Diazepam in vivo and in vitro.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Human hepatocellular carcinoma (HCC) is the fifth most common cancer and the third leading cause of death across the world. Recent evidence suggests that STAT3 regulates proliferative, survival, metastasis, and angiogenesis genes in HCC. Novel agents that suppress STAT3 activation can be used to prevent or treat HCC. We used a functional proteomics tumor pathway technology platform and multiple HCC cell lines to investigate the effects of acacetin (ACN) on STAT3 activation, protein kinases, phosphatases, products of STAT3-regulated genes, and apoptosis. ACN was found to inhibit STAT3 activation in a dose- and time-dependent manner in HCC cells. Upstream kinases c-Src, Janus-activated kinase 1, and Janus-activated kinase 2 were also inhibited. The ACN inhibition of STAT3 was abolished by vanadate treatment, suggesting the involvement of tyrosine phosphatase activity. ACN was found to suppress the protein expression of genes involved in proliferation, survival, and angiogenesis via STAT3 inhibition. ACN appears to be a novel STAT3 inhibitor and may be a promising therapeutic compound for application in the treatment of HCC and other cancers.
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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.