Abstract
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.
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