Cinnamomum cassia essential oil and its major constituent cinnamaldehyde induced cell cycle arrest and apoptosis in human oral squamous cell carcinoma HSC‐3 cells. Issue 2 (25th February 2016)

• Record Type: Journal Article
• Authors: Chang, Wen‐Lun; Cheng, Fu‐Chou; Wang, Shu‐Ping; Chou, Su‐Tze; Shih, Ying
• Is Part Of: Environmental toxicology. Volume 32:Issue 2(2017)
• Page Start: 456
• Page End: 468
• Publication Date: 2016-02-25
• Subjects: Cinnamomum cassia -- essential oil -- cinnamaldehyde -- oral cancer -- HSC‐3 -- apoptosis; Water quality bioassay -- Periodicals; Water -- Pollution -- Toxicology -- Periodicals; Microbiological assay -- Periodicals; Toxicity testing -- Periodicals; Environmental toxicology -- Periodicals; Environmental Pollution -- Periodicals; Environmental Pollutants -- Periodicals; Environmental Monitoring -- Periodicals; Écotoxicologie -- Périodiques; Pollution -- Périodiques; 615.902
• DOI: 10.1002/tox.22250
• Languages: English
• ISSNs: 1520-4081

Abstract

ABSTRACT: Cinnamomum cassia essential oil (CC‐EO) has various functional properties, such as anti‐microbial, hypouricemic, anti‐tyrosinase and anti‐melanogenesis activities. The present study aimed to evaluate the anti‐cancer activities of CC‐EO and its major constituent, cinnamaldehyde, in human oral squamous cell carcinoma HSC‐3 cells. Determination of the cell viability, apoptotic characteristics, DNA damage, cell cycle analysis, reactive oxygen species (ROS) production, mitochondrial membrane potential, cytosolic Ca 2+ level and intracellular redox status were performed. Our results demonstrated that CC‐EO and cinnamaldehyde significantly decreased cell viability and caused morphological changes. The cell cycle analysis revealed that CC‐EO and cinnamaldehyde induced G2/M cell cycle arrest in HSC‐3 cells. The apoptotic characteristics (DNA laddering and chromatin condensation) and DNA damage were observed in the CC‐EO‐treated and cinnamaldehyde‐treated HSC‐3 cells. Moreover, CC‐EO and cinnamaldehyde promoted an increase in cytosolic Ca 2+ levels, induced mitochondrial dysfunction and activated cytochrome c release. The results of ROS production and intracellular redox status demonstrated that CC‐EO and cinnamaldehyde significantly increased the ROS production and thiobarbituric acid reactive substance levels, and the cellular glutathione content and glutathione peroxidase activity were significantly reduced in HSC‐3 cells. Our results suggest that CC‐EO and cinnamaldehyde may possess anti‐oral cancer activity in HSC‐3 cells. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 456–468, 2017.