Journal ArticleDOI
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 +7 more
TLDR
Findings indicate that licochalcone A exerts a cytostatic effect through apoptosis by targeting the JNK/p38 pathway in human nasopharyngeal carcinoma cells, and is a promising therapeutic agent for the treatment of human nasophileal cancer cells.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.read more
Citations
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Journal ArticleDOI
Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma
Lesley Jia Wei Pua,Chun-Wai Mai,Felicia Fei-Lei Chung,Alan Soo Beng Khoo,Chee-Onn Leong,Wei-Meng Lim,Ling-Wei Hii +6 more
TL;DR: This work aims to inspire future studies further delineating JNK and p38 MAPK signaling in NPC oncogenesis which might offer important insights for better strategies in diagnosis, prognosis, and treatment decision-making in NPC patients.
Journal ArticleDOI
Anti-Proliferative and Pro-Apoptotic Effects of Licochalcone A through ROS-Mediated Cell Cycle Arrest and Apoptosis in Human Bladder Cancer Cells
Su Hyun Hong,Hee-Jae Cha,Hyun Hwangbo,Hyun Hwangbo,Min Yeong Kim,SoYoung Kim,SoYoung Kim,Seon Yeong Ji,JaeHun Cheong,Cheol Park,Hyesook Lee,Gi-Young Kim,Sung-Kwon Moon,Seok Joong Yun,Young-Chae Chang,Wun-Jae Kim,Yung Hyun Choi +16 more
TL;DR: The present data indicate that LCA can inhibit the proliferation of human bladder cancer cells by inducing ROS-dependent G2/M phase arrest and apoptosis.
Journal ArticleDOI
Licochalcone A-Induced Apoptosis Through the Activation of p38MAPK Pathway Mediated Mitochondrial Pathways of Apoptosis in Human Osteosarcoma Cells In Vitro and In Vivo
Renn-Chia Lin,Shun-Fa Yang,Hui-Ling Chiou,Shu-Ching Hsieh,Shiua-Hua Wen,Ko-Hsiu Lu,Yi-Hsien Hsieh +6 more
TL;DR: It is demonstrated that LicA has antitumor activities against human osteosarcoma cells through p38MAPK regulation of mitochondria-mediated intrinsic apoptotic pathways in vitro and in vivo.
Journal ArticleDOI
Anticancer Activity of Natural and Synthetic Chalcones.
TL;DR: A huge number of chalcone derivatives with residues such as diaryl ether, sulfonamide, and amine have been obtained, their presence being favorable for anticancer activity as mentioned in this paper.
Journal ArticleDOI
Licochalcone A Suppresses the Proliferation of Osteosarcoma Cells through Autophagy and ATM-Chk2 Activation.
TL;DR: The data indicate that the activation of ATM-Chk2 checkpoint pathway and autophagy may contribute to Licochalcone A-induced anti-proliferating effect in osteosarcoma cell lines.
References
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