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张力蛋白在恶性肿瘤中的作用。

The role of tensins in malignant neoplasms.

作者信息

Nizioł Marcin, Pryczynicz Anna

机构信息

Department of General Pathomorphology, Medical University of Bialystok, Bialystok, Poland.

出版信息

Arch Med Sci. 2021 Jan 26;19(5):1382-1397. doi: 10.5114/aoms/127085. eCollection 2023.

DOI:10.5114/aoms/127085
PMID:37732046
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10507764/
Abstract

Tensins belong to the family of adhesion proteins which form focal adhesions serving as a bridge between the extracellular matrix and intracellular actin skeleton. The tensin family consists of four members (tensin-1 to -4) which are widely expressed in normal and cancerous tissues. The presence of Src homology 2 and phosphotyrosine binding domains is a unique feature of tensins which enables them to interact with tyrosine-phosphorylated proteins in PI3K/Akt and β-integrin/FAK signaling pathways. The tensin-mediated signaling pathway regulates physiological processes including cell motility and cytoskeleton integrity. The expression of tensins varies among cancers. Several papers report tensins as tumor suppressive proteins, whereas tensins may promote epithelial to mesenchymal transition and cancer cell metastasis. Recent findings and further research on tensins as therapeutic targets in cancers may contribute to identifying effective anti-cancer therapy. In this review we focus on the role of tensins in normal and cancer cells. We discuss potential mechanism(s) involved in carcinogenesis.

摘要

张力蛋白属于黏附蛋白家族,该家族形成黏着斑,作为细胞外基质与细胞内肌动蛋白骨架之间的桥梁。张力蛋白家族由四个成员(张力蛋白-1至-4)组成,它们在正常组织和癌组织中广泛表达。Src同源2结构域和磷酸酪氨酸结合结构域的存在是张力蛋白的独特特征,这使得它们能够在PI3K/Akt和β-整合素/FAK信号通路中与酪氨酸磷酸化蛋白相互作用。张力蛋白介导的信号通路调节包括细胞运动和细胞骨架完整性在内的生理过程。张力蛋白的表达在不同癌症中有所不同。几篇论文将张力蛋白报道为肿瘤抑制蛋白,而张力蛋白可能促进上皮-间质转化和癌细胞转移。关于张力蛋白作为癌症治疗靶点的最新发现和进一步研究可能有助于确定有效的抗癌疗法。在这篇综述中,我们重点关注张力蛋白在正常细胞和癌细胞中的作用。我们讨论了致癌过程中涉及的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b591/10507764/e9005ff334d7/AMS-19-5-127085-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b591/10507764/880eb8d9de85/AMS-19-5-127085-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b591/10507764/e9005ff334d7/AMS-19-5-127085-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b591/10507764/880eb8d9de85/AMS-19-5-127085-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b591/10507764/e9005ff334d7/AMS-19-5-127085-g002.jpg

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