期刊
CANCER MANAGEMENT AND RESEARCH
卷 11, 期 -, 页码 8947-8963出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/CMAR.S225606
关键词
E-cadherin; HCC; genetic alterations; epigenetic alterations
类别
资金
- National Natural Science Foundation of China [81872297, 81874059]
- Zhejiang Province Analysis and Test Technology Project [2018C37062]
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.
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