Wang Dong, Han Sheng, Peng Rui, Wang Xing, Yang Xin-Xiang, Yang Ren-Jie, Jiao Chen-Yu, Ding Dong, Ji Gu-Wei, Li Xiang-Cheng
Liver Transplantation Center, First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, Ministry of Public Health, Nanjing, China.
Liver Transplantation Center, First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, Ministry of Public Health, Nanjing, China.
Biochem Biophys Res Commun. 2015 Mar 6;458(2):313-20. doi: 10.1016/j.bbrc.2015.01.108. Epub 2015 Jan 31.
Publicly available microarray data suggests that the expression of FAM83D (Family with sequence similarity 83, member D) is elevated in a wide variety of tumor types, including hepatocellular carcinoma (HCC). However, its role in the pathogenesis of HCC has not been elucidated. Here, we showed that FAM83D was frequently up-regulated in HCC samples. Forced FAM83D expression in HCC cell lines significantly promoted their proliferation and colony formation while FAM83D knockdown resulted in the opposite effects. Mechanistic analyses indicated that FAM83D was able to activate the MEK/ERK signaling pathway and promote the entry into S phase of cell cycle progression. Taken together, these results demonstrate that FAM83D is a novel oncogene in HCC development and may constitute a potential therapeutic target in HCC.
公开可得的微阵列数据表明,FAM83D(序列相似性家族83成员D)在包括肝细胞癌(HCC)在内的多种肿瘤类型中表达升高。然而,其在HCC发病机制中的作用尚未阐明。在此,我们表明FAM83D在HCC样本中经常上调。在HCC细胞系中强制表达FAM83D显著促进其增殖和集落形成,而敲低FAM83D则产生相反的效果。机制分析表明,FAM83D能够激活MEK/ERK信号通路并促进细胞周期进程进入S期。综上所述,这些结果表明FAM83D是HCC发展中的一种新型癌基因,可能构成HCC的潜在治疗靶点。