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Wnt信号通路抑制剂Dickkopf-1在肝癌中的研究进展

Recent Progress of Wnt Pathway Inhibitor Dickkopf-1 in Liver Cancer.

作者信息

Li Jieping, Gong Wenlin, Li Xiaoxue, Wan Ruirong, Mo Fengzhen, Zhang Zhenghua, Huang Panpan, Hu Zixi, Lai Zongqiang, Lu Xiaoling, Zhao Yongxiang

机构信息

National Center for International Research of Biological Targeting Diagnosis and Therapy, Guangxi Key Laboratory of Biological Targeting Diagnosis and Therapy Research, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Medical University, Nanning 530021, Guangxi, China.

出版信息

J Nanosci Nanotechnol. 2018 Aug 1;18(8):5192-5206. doi: 10.1166/jnn.2018.14636.

DOI:10.1166/jnn.2018.14636
PMID:29458569
Abstract

Hepatocellular carcinoma (HCC) is one of the most common cancers around the world. Multiple etiologic factors such as virus and environment can lead to HCC. It is a challenge for us to successfully detect early HCC due to the lack of effective characterized and specific biomarkers. However, if the early diagnosis is successfully realized, it provides crucial chance for HCC patients to receive effective treatment as early as possible. Dickkopf-1 (DKK-1) is a secretary glycoprotein, which negatively regulates Wnt pathway through binding to surface receptors LRP5/6 and Kremen 1/2. The expression of DKK-1 is regulated by p53, V-Myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN), β-catenin, etc. Ectopic expression of DKK-1 can inhibit cell proliferation, or induce apoptosis with apoptosis enhancing factors. DKK-1 is low-expressed in many tumors, but overexpressed in others. Growing evidences show that DKK-1 plays complex and different roles in tumorigenesis, tumor progression and metastasis of different cancers. We herein review the recent progress in the expression and function of DKK-1 in hepatocellular carcinoma.

摘要

肝细胞癌(HCC)是全球最常见的癌症之一。病毒和环境等多种病因可导致HCC。由于缺乏有效的特征性和特异性生物标志物,成功检测早期HCC对我们来说是一项挑战。然而,如果能够成功实现早期诊断,将为HCC患者尽早接受有效治疗提供关键机会。Dickkopf-1(DKK-1)是一种分泌型糖蛋白,它通过与表面受体LRP5/6和Kremen 1/2结合来负向调节Wnt通路。DKK-1的表达受p53、V-Myc禽成髓细胞瘤病毒癌基因神经母细胞瘤衍生同源物(MYCN)、β-连环蛋白等调控。DKK-1的异位表达可抑制细胞增殖,或与凋亡增强因子一起诱导细胞凋亡。DKK-1在许多肿瘤中表达较低,但在其他肿瘤中高表达。越来越多的证据表明,DKK-1在不同癌症的肿瘤发生、肿瘤进展和转移中发挥着复杂而不同的作用。我们在此综述DKK-1在肝细胞癌中的表达和功能的最新进展。

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