[CAS NO. 499-44-5]  β-thujaplicin

In lung cancer cells, hinokitiol inhibits cell proliferation by inducing the p53-independent DNA damage response, autophagy (not apoptosis), S-phase cell cycle arrest, and senescence. Hinokitiol induces autophagy in lung adenocarcinoma cells but not in human lung stromal fibroblasts. It induces cellular senescence in both human lung cancer cells and lung stromal fibroblasts. Treatment with hinokitiol reveals a concentration-dependent inhibition of migration of B16-F10 melanoma cells. It appears to achieve this effect by reducing the expression of MMP-1 and by suppressing the phosphorylation of mitogen- activated protein kinase (MAPK) signaling molecules such as extracellular signal-regulated kinase (ERK) 1/2, p38 MAPK and c-Jun N-terminal kinases (JNK). On the other hand, hinokitiol treatment reverses IκB-α degradation and inhibits the phosphorylation of p65 nuclear factor kappa B (NF-κB) and cJun in B16-F10 cells. In addition, hinokitiol suppresses the translocation of p65 NF-κB from the cytosol to the nucleus, suggesting reduced NF-κB activation.