CHENG-CHIA YU2026-10-162026-10-162015-05-01Pure ID: 15213615Pure UUID: 037b4860-fda5-4ab9-bc43-7ae588c480a910.1016/j.jff.2015.03.036https://www.scopus.com/pages/publications/84929237146https://scholars.csmu.edu.tw/handle/123456789/33384Hinokitiol is reported to inhibit oral squamous cell carcinoma cells growth but its mechanism of action remains unclear. Hinokitiol induced cell cycle arrest in G1 or G1/S phase and induced cell apoptosis in oral squamous cell carcinoma cells. The cDNA microarray data showed 6.25-12.5 μM hinokitiol suppressed pan-histone mRNA expression and quantitative RT-PCR and western blotting showed the reproducibility of the results. Hinokitiol impaired the chromatin folding in oral squamous cell carcinoma cells. In addition, the binding of FLICE-associated huge protein and nuclear protein of the ataxia telangiectasia mutated locus on histone H4/e promoter was decreased, and H4/e promoter activity was significantly decreased. The malignant phenotypes of oral squamous cell carcinoma cells were suppressed in low dose (0.75-6.25 μM hinokitiol) in vitro. Feeding 10 mg/kg hinokitiol to mice suppressed xenograft tumourigenicity of HSC-3 cells in vivo. Hinokitiol showed the efficacy against oral squamous cell carcinoma cells growth by pan-histone suppression.12enjournal article