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Title: Apigenin Inhibits IL-6 Transcription and Suppresses Esophageal Carcinogenesis.

Authors: Qiu, Jian-Ge; Wang, Lin; Liu, Wen-Jing; Wang, Ju-Feng; Zhao, Er-Jiang; Zhou, Feng-Mei; Ji, Xiang-Bo; Wang, Li-Hong; Xia, Zhong-Kun; Wang, Wei; Lin, Marie Chia-Mi; Liu, Ling-Zhi; Huang, Ying-Xue; Jiang, Bing-Hua

Published In Front Pharmacol, (2019)

Abstract: Esophagus cancer is the seventh cause of cancer-related deaths globally. In this study, we analyzed interleukin 6 (IL-6) gene expression in human esophagus cancer patients and showed that IL-6 mRNA levels are significantly higher in tumor tissues and negatively correlated with overall survival, suggesting that IL-6 is a potential therapeutic target for esophagus cancer. We further demonstrated that apigenin, a nature flavone product of green plants, inhibited IL-6 transcription and gene expression in human esophagus cancer Eca-109 and Kyse-30 cells. Apigenin significantly and dose-dependently inhibited cell proliferation and promoted apoptosis while stimulating the cleaved PARP (poly ADP-ribose polymerase) (C-PARP) and caspase-8 expression. It suppressed VEGF (Vascular endothelial growth Factor) expression and tumor-induced angiogenesis. Pretreatment of cells with IL-6 could completely reverse apigenin-induced cellular changes. Finally, using a preclinical nude mice model subcutaneously xenografted with Eca-109 cells, we demonstrated the in vivo antitumor activity and mechanisms of apigenin. Taken together, this study revealed for the first time that apigenin is a new IL-6 transcription inhibitor and that inhibiting IL-6 transcription is one of the mechanisms by which apigenin exhibits its anticancer effects. The potential clinical applications of apigenin in treating esophagus cancer warrant further investigations.

PubMed ID: 31572184 Exiting the NIEHS site

MeSH Terms: No MeSH terms associated with this publication

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