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Cellular function assays showed that higher levels of UNC119 not only promoted proliferation but also enhanced HCC cell migration and invasion. UNC119 promoted progression of the cell cycle and significantly promoted HCC cell growth through the Wnt/β-catenin signal pathway, and enhanced tumor migration and invasion by the TGF-β/EMT pathway. Curcumin efficiently inhibited HCC cell proliferation by blocking the Wnt/β-catenin pathway and inhabited migration and invasion by blocking the TGF-p/EMT signal pathway. Curcumin not only was beneficial for tumor remission but also contributed to the long-term survival of HCC-bearing mice. UNC119 was significantly upregulated and promoted cell growth in hepatic cancer cells and tissues by the Wnt/β-catenin signal pathway and migration by TGF-β/EMT signal pathway. 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引用次数: 11

摘要

据报道,UNCI 19在肝癌细胞(HCC)中的表达显著升高。然而,调节UNC119在HCC中的表达的临床意义尚不清楚。本研究旨在探讨姜黄素在HCC细胞系和组织中调节UNC119表达的潜力,方法包括定量实时PCR、western blot和免疫组织化学分析。体外和体内分析UNC119在肿瘤细胞增殖、生长和周期中的生物学功能。与正常肝细胞和组织相比,HCC细胞系和组织中UNC119的表达上调。细胞功能分析显示,高水平的UNC119不仅促进了细胞增殖,而且增强了HCC细胞的迁移和侵袭。UNC119通过Wnt/β-catenin信号通路促进细胞周期进展,显著促进HCC细胞生长,通过TGF-β/EMT通路增强肿瘤迁移侵袭。姜黄素通过阻断Wnt/β-catenin通路有效抑制肝癌细胞增殖,通过阻断TGF-p/EMT信号通路有效抑制肝癌细胞的迁移和侵袭。姜黄素不仅有利于肿瘤缓解,而且有助于肝癌小鼠的长期生存。UNC119在肝癌细胞和组织中通过Wnt/β-catenin信号通路显著上调,促进细胞生长,通过TGF-β/EMT信号通路促进细胞迁移。姜黄素通过抑制这些途径抑制细胞增殖、生长、迁移和侵袭。
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Curcumin Modulates Hepatocellular Carcinoma by Reducing UNC119 Expression.
UNCI 19 expression has been reported to be significantly higher in hepatic cancer cells (HCC). However, the clinical significance of modulating UNC119 expression in HCC is not well understood. The study described here aimed to explore the potential of curcumin in modulation of UNC119 expression in HCC by assessment with quantitative real-time PCR, western blot, and immune-histochemical analyses in HCC cell lines and tissues. The biological functions of UNC119 in the proliferation, growth, and cycle of tumor cells were analyzed both in vitro and in vivo. UNC119 expression was upregulated in HCC cell lines and tissues as indicated by comparison with normal liver cells and tissues. Cellular function assays showed that higher levels of UNC119 not only promoted proliferation but also enhanced HCC cell migration and invasion. UNC119 promoted progression of the cell cycle and significantly promoted HCC cell growth through the Wnt/β-catenin signal pathway, and enhanced tumor migration and invasion by the TGF-β/EMT pathway. Curcumin efficiently inhibited HCC cell proliferation by blocking the Wnt/β-catenin pathway and inhabited migration and invasion by blocking the TGF-p/EMT signal pathway. Curcumin not only was beneficial for tumor remission but also contributed to the long-term survival of HCC-bearing mice. UNC119 was significantly upregulated and promoted cell growth in hepatic cancer cells and tissues by the Wnt/β-catenin signal pathway and migration by TGF-β/EMT signal pathway. Curcumin treatment inhibited cell proliferation, growth, migration, and invasion by inhibition of those pathways.
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