The anticancer mechanism of 2'-hydroxycinnamaldehyde in human head and neck cancer cells.

Abstract

Cinnamaldehyde has been shown to effectively induce apoptosis in a number of human cancer cells. In the present study, cinnamaldehyde derivative-induced apoptosis and its signaling pathways were assessed in p53-wild (SGT) and p53-mutant (YD-10B) human head and neck cancer cells. The cinnamaldehyde derivatives, 2'-hydroxycinnamaldehyde (HCA) and 2'-benzoyloxycinnamaldehyde (BCA), exhibited powerful anti-proliferative effects on SGT and YD-10B cells. The apoptotic effect induced by HCA or BCA was supported by caspase-3, -7, -9 and PARP activation, and confirmed by Annexin V-FITC/PI double staining. HCA induced the expression of p21 in both SGT and YD-10B cells. Furthermore, HCA induced the level of pro-apoptotic Bak1 expression while decreasing the level of anti-apoptotic Bcl-2 in both cell lines, suggesting that HCA induced the cell death pathway in a p53-independent manner. HCA also induced the expression of LC3B in SGT and YD-10B cells. Following pre-incubation with the autophagy inhibitor 3-MA, HCA-induced apoptosis was largely increased in SGT cells, while inhibited in YD-10B cells, suggesting that autophagy may actively contribute to HCA-induced apoptosis. Taken together, these observations suggest that HCA may be an effective therapeutic agent in the treatment of head and neck cancer regardless of p53 status.

• Authors: Sang-Gun Ahn, Young-Hee Jin, Jung-Hoon Yoon, Soo-A Kim
• Journal: International journal of oncology (Int J Oncol) Vol. 47 Issue 5 Pg. 1793-800 (Nov 2015) ISSN: 1791-2423 [Electronic] Greece
• PMID: 26352194 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Annexin A5
• Cinnamates
• Reactive Oxygen Species
• p-hydroxycinnamaldehyde

Topics

• Annexin A5 (metabolism)
• Apoptosis (drug effects)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cinnamates (administration & dosage)
• Head and Neck Neoplasms (drug therapy, metabolism, pathology)
• Humans
• Reactive Oxygen Species (metabolism)
• Signal Transduction (drug effects)