ArticleCell & bioscience2014
Pinocembrin suppresses TGF-β1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating αvβ3 integrin/FAK/p38α signaling pathway.
Article in Cell & bioscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 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
- Integrin β3: structural functions, tumour microenvironment regulatory roles and targeted intervention strategies.Frontiers in immunology · 2026Review
- Pinocembrin as a novel anti-cancer agent: Exploring preclinical evidence along with therapeutic potential.World journal of experimental medicine · 2025Review
- Pinocembrin Downregulates Vascular Smooth Muscle Cells Proliferation and Migration Leading to Attenuate Neointima Formation in Balloon-Injured Rats.Biomolecules · 2025Article
- Immunohistochemistry identifies E-cadherin, N-cadherin and focal adhesion kinase (FAK) as predictors of stage I non-small cell lung carcinoma spread through the air spaces (STAS), and the combinations as prognostic factors.Translational lung cancer research · 2024Article
- Molecular and Cellular Mechanisms of Propolis and Its Polyphenolic Compounds against Cancer.International journal of molecular sciences · 2022Review
- Article
- Advances in the research of plant-derived natural products against retinoblastoma.International journal of ophthalmology · 2022Review
- Chinese Propolis Suppressed Pancreatic Cancer Panc-1 Cells Proliferation and Migration via Hippo-YAP Pathway.Molecules (Basel, Switzerland) · 2021Article
- An innovative cell model revealed the inhibitory effect of flavanone structure on peroxynitrite production through interaction with the IKKβ kinase domain at ATP binding site.Food science & nutrition · 2020Article
- ITGB3/CD61: a hub modulator and target in the tumor microenvironment.American journal of translational research · 2019Review
- Lippia origanoides extract induces cell cycle arrest and apoptosis and suppresses NF-κB signaling in triple-negative breast cancer cells.International journal of oncology · 2017Article
- Integrin β4 promotes cell invasion and epithelial-mesenchymal transition through the modulation of Slug expression in hepatocellular carcinoma.Scientific reports · 2017Article
- Recent Pathophysiological Aspects of Peyronie's Disease: Role of Free Radicals, Rationale, and Therapeutic Implications for Antioxidant Treatment-Literature Review.Advances in urology · 2017Review
- Anti-proliferative Effects of Pinocembrin Isolated FromIntegrative cancer therapiesArticle
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPinocembrin is the most abundant flavonoid in propolis. In this study, we investigated the antimetastatic effect of pinocembrin on TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of human Y-79 retinoblastoma cells.
resultsFirstly, the results showed that pinocembrin significantly suppresses the TGF-β1-induced abilities of the invasion and migration of Y-79 cells under non-cytotoxic concentration. Pinocembrin decreased TGF-β1-induced expression of vimentin, N-cadherin, αv and β3 integrin in Y-79 cells. Molecular data also showed pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38α signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-β1. Next, pinocembrin also strongly inhibited the degradation of inhibitor of kappaBα (IκBα) and the nuclear levels of nuclear factor kappa B (NF-κB). Also, a dose-dependent inhibition on the binding ability of NF-κB was further observed under pinocembrin treatment.
conclusionsPresented results indicated that pinocembrin inhibits TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the αvβ3 integrin/FAK/p38α signaling pathway. Thus, our findings point to the anticancer potential of pinocembrin against retinoblastoma cells.
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