In vitro activity: Curcumol induced cell death in human lung adenocarcinoma (ASTC-a-1) cells by inducing G(2)/M phase arrest, nuclear fragmentation, phosphatidylserine externalization and a rapid translocation of Bax from cytosol into mitochondria. While, caspases are not involved in Curcumol-induced apoptosis. Curcumol also benefits rheumatoid arthritis treatment through suppressing the fibroblast-like synoviocytes (FLS) proliferation and DNA synthesis. It attenuates PDGF-BB-induced Jak2 phosphorylation and downregulates STAT1 and STAT3 DNA-binding activities.

Cell Assay: Curcumol exhibited time- and concentration-dependent anti-proliferative effects in SPC-A-1 human lung adenocarcinoma cells with cell cycle arrest in the G0/G1 phase while apoptosis-induction was also confirmed with flow cytometry and morphological analyses. Curcumol-induced growth inhibition correlated with apoptosis induction as evidenced by Annexin V staining, and cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP) in HSC-T6. Suppression of the NF-κB translocation via inhibition of IκB-α phosphorylation by the curcumol led to the inhibition of expression of NF-κB-regulated gene, e.g. Bcl-xL and Bcl-2, in a PI3K-dependent manner, which is upstream of NF-κB activation. Curcumol exhibits an inhibitory effect on receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast differentiation with both bone marrow-derived macrophages and RAW264.7 cells in a dose-dependent manner.

Med Oncol. 2011 Mar;28(1):307-14; Evid Based Complement Alternat Med. 2012;2012:746426; Asian Pac J Cancer Prev. 2015;16(6):2307-12.