Licochalcone A inhibits growth of gastric cancer cells by arresting cell cycle progression and inducing apoptosis

• Published in: Cancer letters Vol. 302; no. 1; pp. 69 - 75
• Main Authors: Xiao, Xiu-ying, Hao, Miao, Yang, Xin-ying, Ba, Qian, Li, Mian, Ni, Shu-juan, Wang, Li-Sha, Du, Xiang
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 01.03.2011; Elsevier Limited
• Subjects: Acids; anticarcinogenic activity; Apoptosis; Apoptosis - drug effects; Apoptosis Regulatory Proteins - metabolism; Blotting, Western; Cancer therapies; caspase-3; Cell cycle; Cell Cycle - drug effects; Cell Cycle Proteins - metabolism; Cell Division - drug effects; cell growth; Cell Line; Cell Line, Tumor; Cell Proliferation - drug effects; Cell viability; Chalcones - chemistry; Chalcones - pharmacology; Cytotoxicity; Dose-Response Relationship, Drug; epithelium; G2 Phase - drug effects; Gastric cancer; Glycyrrhiza - chemistry; Hematology, Oncology and Palliative Medicine; Humans; Inhibitory Concentration 50; Licochalcone A; licorice; mechanism of action; Medical prognosis; Molecular Structure; Mortality; Phase transitions; stomach neoplasms; Stomach Neoplasms - metabolism; Stomach Neoplasms - pathology; Cell viability; Licochalcone A; Gastric cancer; Cell cycle; Apoptosis
• ISSN: 0304-3835; 1872-7980
• DOI: 10.1016/j.canlet.2010.12.016

Abstract The aim of this study was to determine the anticancer effects of seven licorice compounds in MKN-28, AGS, and MKN-45 gastric cancer cells and human gastric epithelium immortalized cells. We also explored the mechanism of action of licochalcone A (LCA), the most cytotoxic licorice compound, by analyzing its influence on cell cycle progression and apoptosis. The results indicated that LCA was the most cytotoxic licorice compound of those tested, and it inhibited gastric cancer cells growth in a dose-dependent manner, with an IC50 value of approximately 40 μM. LCA affected gastric cancer cell viability by blocking cell cycle progression at the G2/M transition and inducing apoptosis. LCA treatment increased the expression of Rb and decreased the expression of cyclin A, cyclin B and MDM2 in MKN-28, AGS and MKN-45 cell lines. In addition, LCA-induced apoptosis by its effects on the expression of PARP, caspase-3, Bcl-2 and Bax. These data provide evidence that LCA has the potential to be used in the treatment of gastric cancer.