Homoharringtonine suppresses tumor proliferation and migration by regulating EphB4-mediated β-catenin loss in hepatocellular carcinoma.

作者: Man Zhu , Zhengyan Gong , Qing Wu , Qi Su , Tianfeng Yang

DOI: 10.1038/S41419-020-02902-2

关键词:

摘要: Overexpressed EphB4 conduce to tumor development and is regarded as a potential anticancer target. Homoharringtonine (HHT) has been approved for hematologic malignancies treatment, but its effect on hepatocellular carcinoma (HCC) not studied. This study elucidated HHT could restrain the proliferation migration of HCC via an EphB4/β-catenin-dependent manner. We found that antiproliferative activity in cells xenograft was closely related expression. In HepG2, Hep3B SMMC-7721 cells, overexpression or EphrinB2 Fc stimulation augmented HHT-induced inhibitory cell growth ability, such abrogated when knocked down. The similar observed EphB4+/SMMC-7721 vivo. Preliminary mechanistic investigation indicated directly bound suppressed Data obtained from patients revealed increased β-catenin expression positive correlation between levels. suppression promoted phosphorylation loss β-catenin, which triggered regulation downstream signaling migration, resulting reversion EMT TGF-β-induced HepG2 cells. Collectively, this provided groundwork effective antitumor agent

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