紧密连接蛋白与肝细胞癌。

Claudins and hepatocellular carcinoma.

机构信息

The Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, 126 Xinmin Avenue, Changchun, Jilin 130021, China; The Second Norman Bethune College of Clinical Medicine, Jilin University, Changchun 130021, China.

The Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, 126 Xinmin Avenue, Changchun, Jilin 130021, China; The First Norman Bethune College of Clinical Medicine, Jilin University, Changchun 130021, China.

出版信息

Biomed Pharmacother. 2024 Feb;171:116109. doi: 10.1016/j.biopha.2023.116109. Epub 2024 Jan 6.

DOI:10.1016/j.biopha.2023.116109

PMID:38185042

Abstract

Hepatocellular carcinoma (HCC) has a high incidence and dismal prognosis, making it a significant global health burden. To change this, the development of new therapeutic strategies is imminent. The claudin (CLDN) family, as key components of tight junctions (TJs), plays an important role in the initiation and development of cancer. Dysregulated expression of CLDNs leads to loss of intercellular adhesion and aberrant cell signaling, which are closely related to cancer cell invasion, migration, and epithelial-mesenchymal transition (EMT). CLDN1, CLDN3, CLDN4, CLDN5, CLDN6, CLDN7, CLDN9, CLDN10, CLDN11, CLDN14, and CLDN17 are aberrantly expressed in HCC, which drives the progression of the disease. Consequently, they have tremendous potential as prognostic indicators and therapeutic targets. This article summarizes the aberrant expression, molecular mechanisms, and clinical application studies of different subtypes of CLDNs in HCC, with a particular emphasis on CLDN1.

摘要

肝细胞癌（HCC）发病率高，预后差，是全球重大的健康负担。为改变这一现状，迫切需要开发新的治疗策略。紧密连接（TJ）的关键组成部分 Claudin（CLDN）家族在癌症的发生和发展中发挥着重要作用。CLDN 的表达失调导致细胞间黏附丧失和异常的细胞信号转导，这与癌细胞的侵袭、迁移和上皮-间充质转化（EMT）密切相关。CLDN1、CLDN3、CLDN4、CLDN5、CLDN6、CLDN7、CLDN9、CLDN10、CLDN11、CLDN14 和 CLDN17 在 HCC 中异常表达，驱动疾病的进展。因此，它们作为预后指标和治疗靶点具有巨大的潜力。本文总结了不同亚型的 CLDN 在 HCC 中的异常表达、分子机制和临床应用研究，特别强调了 CLDN1。