https://scholars.lib.ntu.edu.tw/handle/123456789/392612
標題: | Honokiol from Magnolia spp. induces G1 arrest via disruption of EGFR stability through repressing HDAC6 deacetylated Hsp90 function in lung cancer cells | 作者: | Liou, S.-F. KUO-TAI HUA Hsu, C.-Y. Weng, M.-S. |
關鍵字: | Epidermal growth factor receptor (EGFR); Heat-shock protein 90 (Hsp90); Histone deacetylase 6 (HDAC6); Honokiol; Hyper-acetylation | 公開日期: | 2015 | 卷: | 15 | 起(迄)頁: | 84-96 | 來源出版物: | Journal of Functional Foods | 摘要: | Honokiol, an active compound derived from Magnolia spp. bark, possesses chemopreventive properties in many cancer cell models. However, the chemopreventive mechanism of honokiol in lung cancer cells is still a mystery. We examined histone deacetylase 6 (HDAC6)-mediated epidermal growth factor receptor (EGFR) stability in honokiol-treated lung cancer cells. The results showed that honokiol induced G1 growth arrest was through down-regulation of EGFR expression and thereafter downstream signaling pathways. HDAC6 activity was directly inhibited via honokiol at IC50 about 23.55 ± 1.18 μM. Inhibition of HDAC6 activity via honokiol was followed by disrupting HDAC6 and heat shock protein 90 (Hsp90) association and resulting in Hsp90 hyper-acetylation. Meanwhile, hyper-acetylated Hsp90 had been found to disassociate with EGFR and followed by EGFR degradation. Taken together, these results suggested that interruption of EGFR stability by honokiol was through inhibiting HDAC6 activity and consequently suppressing Hsp90 chaperon function in lung cancer cells. ? 2015 Elsevier Ltd. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84929241490&partnerID=40&md5=5107e38c93890487db4ba9160dc20e3e http://scholars.lib.ntu.edu.tw/handle/123456789/392612 |
DOI: | 10.1016/j.jff.2015.03.018 | SDG/關鍵字: | Magnolia |
顯示於: | 毒理學研究所 |
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