Toxicology (Amsterdam), 2014-12, Vol.326, p.9-17
2014
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- Autor(en) / Beteiligte
- Titel
- Galangin suppresses HepG2 cell proliferation by activating the TGF-β receptor/Smad pathway
- Ist Teil von
- Toxicology (Amsterdam), 2014-12, Vol.326, p.9-17
- Ort / Verlag
- Ireland: Elsevier Ireland Ltd
- Erscheinungsjahr
- 2014
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Abstract Galangin can suppress hepatocellular carcinoma (HCC) cell proliferation. In this study, we demonstrated that galangin induced autophagy by activating the transforming growth factor (TGF)-β receptor/Smad pathway and increased TGF-β receptor I (RI), TGF-βRII, Smad1, Smad2, Smad3 and Smad4 levels but decreased Smad6 and Smad7 levels. Autophagy induced by galangin appears to depend on the TGF-β receptor/Smad signalling pathway because the down-regulation of Smad4 by siRNA or inhibition of TGF-β receptor activation by LY2109761 blocked galangin-induced autophagy. The down-regulation of Beclin1, autophagy-related gene (ATG) 16L, ATG12 and ATG3 restored HepG2 cell proliferation and prevented galangin-induced apoptosis. Our findings indicate a novel mechanism for galangin-induced autophagy via activation of the TGF-β receptor/Smad pathway. The induction of autophagy thus reflects the anti-proliferation effect of galangin on HCC cells.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0300-483XeISSN: 1879-3185DOI: 10.1016/j.tox.2014.09.010Titel-ID: cdi_proquest_miscellaneous_1660096962
- Format
- –
- Schlagworte
- Activation, Antineoplastic Agents - pharmacology, Apoptosis - drug effects, Apoptosis Regulatory Proteins - metabolism, Autophagy, Autophagy - drug effects, Autophagy-related gene, Blocking, Carcinoma, Hepatocellular - genetics, Carcinoma, Hepatocellular - metabolism, Carcinoma, Hepatocellular - pathology, Cell Proliferation - drug effects, Dose-Response Relationship, Drug, Emergency, Flavonoids - pharmacology, Galangin, Genes, Growth factors, Hep G2 Cells, Humans, Inhibition, Liver Neoplasms - genetics, Liver Neoplasms - metabolism, Liver Neoplasms - pathology, Pathways, Protein-Serine-Threonine Kinases - antagonists & inhibitors, Protein-Serine-Threonine Kinases - metabolism, Pyrazoles - pharmacology, Pyrroles - pharmacology, Receptors, Receptors, Transforming Growth Factor beta - antagonists & inhibitors, Receptors, Transforming Growth Factor beta - metabolism, RNA Interference, Signal Transduction - drug effects, Smad, Smad Proteins - genetics, Smad Proteins - metabolism, TGF-β receptor, Toxicology, Transfection, Transforming Growth Factor beta - metabolism