ArticleIntegrative cancer therapies
Anti-proliferative Effects of Pinocembrin Isolated From
Article in Integrative cancer therapies. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Pinocembrin, an anticancer dihydroxyflavanone: from chemistry to cellular interactions and synergistic prospects.Cancer cell international · 2026Review
- Recent Progress on Polyphenols of Malaysian Honey and Their Molecular Mechanism Pathways in Cancer-A Comprehensive Review.International journal of molecular sciences · 2026Review
- Magnetic domain orientation in magnetite FeRSC advances · 2026Article
- Effective Components and Molecular Mechanism of Biejiaruangan Capsule Against Liver Fibrosis: High-resolution Mass Spectrometry, Network Pharmacological Analysis and Experimental Verification.Combinatorial chemistry & high throughput screening · 2026Article
- Pinocembrin as a novel anti-cancer agent: Exploring preclinical evidence along with therapeutic potential.World journal of experimental medicine · 2025Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) is the most prevalent primary liver cancer.
methodsDry flowers of
resultsAmong 3 purified flavonoids, pinocembrin, pinostrobin, and chrysin, and 1 indole alkaloid (3-farnesylindole), only pinocembrin showed inhibitory effects on the proliferation of 2 HCC cell lines, HepG2 and Li-7, whereas chrysin showed specific toxicity to HepG2. Pinocembrin was then selected for further study. Flow cytometric analyses revealed that pinocembrin arrested the HCC cell cycle at the G1 phase with a minimal effect on cell death induction. Pinocembrin exerted the suppression of STAT3, as shown by the molecular docking on STAT3 with a better binding affinity than stattic, a known STAT3 inhibitor. Pinocembrin also suppressed STAT3 phosphorylation at both Tyr705 and Ser727. Cell cycle regulatory proteins under the modulation of STAT3, namely cyclin D1, cyclin E, CDK4, and CDK6, are substantially suppressed in their expression levels.
conclusionPinocembrin extracted from
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.