Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma

被引:35
作者
Fan, Xiaoxiao [1 ]
Jin, Shengxi [1 ,2 ]
Li, Yirun [1 ]
Khadaroo, Parikshit Asutosh [2 ,3 ]
Dai, Yili [1 ,2 ]
He, Lifeng [1 ]
Zhou, Daizhan [1 ]
Lin, Hui [1 ]
机构
[1] Zhejiang Univ, Sch Med, Sir Run Run Shaw Hosp, Dept Gen Surg, 3 East Qingchun Rd, Hangzhou 310016, Zhejiang, Peoples R China
[2] Zhejiang Univ, Sch Med, Hangzhou, Zhejiang, Peoples R China
[3] Monash Univ, Sch Publ Hlth & Prevent Med, Melbourne, Vic, Australia
基金
中国国家自然科学基金;
关键词
E-cadherin; HCC; genetic alterations; epigenetic alterations; EPITHELIAL-MESENCHYMAL TRANSITION; HEPATITIS-B-VIRUS; REPRESSES E-CADHERIN; INVASION-SUPPRESSOR GENE; TUMOR-CELL PROLIFERATION; TGF-BETA PROMOTES; NONCODING RNA; DOWN-REGULATION; PROGNOSTIC BIOMARKER; HISTONE METHYLATION;
D O I
10.2147/CMAR.S225606
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.
引用
收藏
页码:8947 / 8963
页数:17
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