Apigenin inhibits NF-κB and Snail signaling, EMT and metastasis in human hepatocellular carcinoma
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Yuan Qin1,2,*, Dong Zhao1,2,*, Hong-gang Zhou1,2,*, Xing-hui Wang3,*, Wei-long Zhong1,2, Shuang Chen2, Wen-guang Gu1,2, Wei Wang1,2, Chun-hong Zhang1,2, Yan-rong Liu2, Hui-juan Liu2, Qiang Zhang1,2, Yuan-qiang Guo1,2, Tao Sun1,2, Cheng Yang1,2
1State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, China
2Tianjin Key Laboratory of Molecular Drug Research, Nankai University and Tianjin International Joint Academy of Biomedicine, Tianjin, China
3Department of Pathology, The People’s Hospital of Shouguang City, Shouguang, Shandong Province, China
*These authors contributed equally to this work
Cheng Yang, email: Cheng.firstname.lastname@example.org
Tao Sun, email: email@example.com
Keywords: apigenin, antitumor, EMT, metastasis, HCC
Received: January 21, 2016 Accepted: April 11, 2016 Published: May 17, 2016
Apigenin is a naturally occurring compound with anti-inflammatory, antioxidant, and anticancer properties. In this study, we investigated the effects of apigenin on migration and metastasis in experimental human hepatocellular carcinoma (HCC) cell lines in vitro and in vivo. Apigenin dose-dependently inhibited proliferation, migration, and invasion by PLC and Bel-7402 human HCC cells. It also suppressed tumor growth in PLC cell xenografts without altering body weight, thereby prolonging survival. Apigenin reduced Snai1 and NF-κB expression, reversed increases in epithelial-mesenchymal transition (EMT) marker levels, increased cellular adhesion, regulated actin polymerization and cell migration, and inhibited invasion and migration by HCC cells. Apigenin may therefore inhibit EMT by inhibiting the NF-κB/Snail pathway in human HCC.
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