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Licochalcone A Induces Apoptotic Cell Death via JNK/p38 Activation in Human Nasopharyngeal Carcinoma Cells

Chun-Yi Chuang, Cheng-Ming Tang, Hsin-Yu Ho, Chung-Han Hsin, Chia-Jui Weng, Shun-Fa Yang, Pei-Ni Chen, Chiao-Wen Lin

Environ Toxicol. 2019 Jul;34(7):853-860.

PMID: 30983163

Abstract:

Licochalcone A is widely studied in different fields and possesses antiasthmatic, antibacterial, anti-inflammatory, antioxidative, and anticancer properties. Its antimalignancy activity on renal, liver, lung, and oral cancer has been explored. However, limited studies have been conducted on the inhibitory effects of licochalcone A in human nasopharyngeal carcinoma cells. We determined cell viability using MTT assay. Cell cycle distribution and apoptotic cell death were measured via flow cytometry. Caspase activation and mitogen-activated protein kinase-related proteins in nasopharyngeal cancer cells in response to licochalcone A were identified by Western blot analysis. Results indicated that licochalcone A reduces cell viability and induces apoptosis, as evidenced by the upregulation of caspase-8 and caspase-9, caspase-3 activation, and cleaved-poly ADP-ribose polymerase expression. Treatment with licochalcone A significantly increases ERK1/2, p38, and JNK1/2 activation. Co-administration of a JNK inhibitor (JNK-IN-8) or p38 inhibitor (SB203580) abolishes the activation of caspase-9, caspase-8, and caspase-3 protein expression during licochalcone A treatment. These findings indicate that licochalcone A exerts a cytostatic effect through apoptosis by targeting the JNK/p38 pathway in human nasopharyngeal carcinoma cells. Therefore, licochalcone A is a promising therapeutic agent for the treatment of human nasopharyngeal cancer cells.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP58749227 Licochalcone A Licochalcone A 58749-22-7 Price
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