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Oncotarget. 2016 Jul 5;7(27):41421-41431. doi: 10.18632/oncotarget.9404.

Apigenin inhibits NF-κB and snail signaling, EMT and metastasis in human hepatocellular carcinoma.

Qin Y1,2, Zhao D1,2, Zhou HG1,2, Wang XH3, Zhong WL1,2, Chen S2, Gu WG1,2, Wang W1,2, Zhang CH1,2, Liu YR2, Liu HJ2, Zhang Q1,2, Guo YQ1,2, Sun T1,2, Yang C1,2.

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State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, China.
Tianjin Key Laboratory of Molecular Drug Research, Nankai University and Tianjin International Joint Academy of Biomedicine, Tianjin, China.
Department of Pathology, The People's Hospital of Shouguang City, Shouguang, Shandong Province, China.


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.


EMT; HCC; antitumor; apigenin; metastasis

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