肝细胞生长因子
DU145型
波形蛋白
上皮-间质转换
蛋白激酶B
癌症研究
PI3K/AKT/mTOR通路
C-Met公司
化学
信号转导
磷酸化
前列腺癌
细胞生物学
生物
癌症
内科学
免疫学
医学
转移
LNCaP公司
生物化学
受体
免疫组织化学
作者
Hsiang‐Yu Chang,Ming‐Ching Kao,Tzong‐Der Way,Chi‐Tang Ho,Earl Fu
摘要
Substantial activation of the hepatocyte growth factor (HGF)/c-Met pathway leads to cancer cell scattering and invasion and has been observed in several types of cancers, including prostate and colorectal cancers. The phosphorylation cascade downstream of HGF, particularly PI3K/Akt signaling, regulates epithelial-to-mesenchymal transition (EMT). How this signaling governs EMT and whether specific kinases respond to particular EMT effectors remain unclear. This study found specific increases in Mdm2 and vimentin rather than the coregulation of an array of EMT marker proteins in response to HGF-induced EMT in DU145 prostate cancer cells. Importantly, it was further found that diosgenin abrogated HGF-induced DU145 cell scattering and invasion. Moreover, diosgenin effectively inhibited the HGF-induced increases in Mdm2 and vimentin by down-regulating phosphorylated Akt and mTOR. In summary, the results suggest that diosgenin may be a potential compound for use in prostate cancer therapy to target the major HGF-induced EMT pathway.
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