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整合素β4(ITGB4)在肿瘤迁移和侵袭中的机制。

The mechanism of ITGB4 in tumor migration and invasion.

作者信息

Huang Guichen, Zhou Minfeng, Lu Damin, Li Jinxiao, Tang Qian, Xiong Chutong, Liang Fengxia, Chen Rui

机构信息

Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

School of Acupuncture and Bone Injury, Hubei University of Chinese Medicine, Wuhan, China.

出版信息

Front Oncol. 2024 Aug 7;14:1421902. doi: 10.3389/fonc.2024.1421902. eCollection 2024.

Abstract

Integrin β4 (ITGB4) is a transmembrane protein that functions as a mechanosensor, mediating the bidirectional exchange of information between the intracellular and extracellular matrices. ITGB4 plays a critical role in cell adhesion, migration, and signaling. Numerous studies have implicated ITGB4 as a key facilitator of tumor migration and invasion. This review provides a foundational description of the mechanisms by which ITGB4 regulates tumor migration and invasion through pathways involving focal adhesion kinase (FAK), protein kinase B (AKT), and matrix metalloproteinases (MMPs). These mechanisms encompass epithelial-mesenchymal transition (EMT), phosphorylation, and methylation of associated molecules. Additionally, this review explores the role of ITGB4 in the migration and invasion of prevalent clinical tumors, including those of the digestive system, breast, and prostate.

摘要

整合素β4(ITGB4)是一种跨膜蛋白,作为一种机械传感器发挥作用,介导细胞内和细胞外基质之间的双向信息交换。ITGB4在细胞黏附、迁移和信号传导中起关键作用。大量研究表明ITGB4是肿瘤迁移和侵袭的关键促进因子。本综述对ITGB4通过涉及粘着斑激酶(FAK)、蛋白激酶B(AKT)和基质金属蛋白酶(MMP)的途径调节肿瘤迁移和侵袭的机制进行了基础描述。这些机制包括上皮-间质转化(EMT)、相关分子的磷酸化和甲基化。此外,本综述还探讨了ITGB4在常见临床肿瘤(包括消化系统、乳腺和前列腺肿瘤)迁移和侵袭中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0db/11335651/642193f5d11d/fonc-14-1421902-g001.jpg

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