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Induction of apoptotic but not autophagic cell death by Cinnamomum cassia extracts on human oral cancer cells
Author(s) -
Yu ChingHan,
Chu ShuChen,
Yang ShunFa,
Hsieh YihShou,
Lee ChihYi,
Chen PeiNi
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27338
Subject(s) - apoptosis , viability assay , cinnamomum , autophagy , pharmacology , cancer cell , cassia , programmed cell death , cancer research , cancer , biology , chemistry , medicine , biochemistry , pathology , traditional chinese medicine , genetics , alternative medicine
Cinnamomum cassia has been widely studied in different fields to reveal its antidiabetic, antidepressive, antiviral, anti‐inflammatory, antiosteoporotic, and anticancer effects. Its antimalignant activities have been explored in lung cancer, breast cancer, colorectal cancer, and even oral cancer, but the detailed signaling mechanism and effects of this plant on animal models need to be clarified. In the current study, C. cassia extract (CCE) was used to investigate the antitumorigenesis mechanism in vitro and in vivo. The major constituents of CCE used in this study were coumarin, cinnamic acid, and cinnamic aldehyde. CCE reduced the viability, number, and colony formation of human oral cancer cells, and induced their apoptosis. Caspase‐3 activation, Bcl‐2 reduction, and phosphatidylserine inversion were involved in CCE‐stimulated apoptosis. CCE also enhanced the expression of autophagic markers, including acidic vesicular organelle, microtubule‐associated protein 1 light chain 3‐I, autophagy‐related protein 14, rubicon, and p62. The combined treatment of CCE and caspase inhibitor significantly restored mitochondrial membrane potential (Δ ψ m ) and cell viability. However, the combined treatment of CCE and autophagy inhibitor further reduced the cell viability indicating that autophagy might be a survival pathway of CCE‐treated SASVO3 cells. In contrast, CCE treatment for 12 days did not adversely affect SASVO3 tumor‐bearing nude mice. CCE also elicited dose‐dependent effects on the decrease in tumor volume, tumor weight, and Ki‐67 expression. These results suggested that CCE showed the potential for the complementary treatment of oral caner.