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肌动蛋白组成重塑作为癌症的一个标志。

The remodelling of actin composition as a hallmark of cancer.

作者信息

Suresh Rahul, Diaz Roberto J

机构信息

Montreal Neurological Institute, Integrated Program in Neuroscience, McGill University, Montreal, Canada.

Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, Faculty of Medicine, McGill University, Montreal, Canada.

出版信息

Transl Oncol. 2021 Jun;14(6):101051. doi: 10.1016/j.tranon.2021.101051. Epub 2021 Mar 21.

DOI:10.1016/j.tranon.2021.101051
PMID:33761369
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8008238/
Abstract

Actin is a key structural protein that makes up the cytoskeleton of cells, and plays a role in functions such as division, migration, and vesicle trafficking. It comprises six different cell-type specific isoforms: ACTA1, ACTA2, ACTB, ACTC1, ACTG1, and ACTG2. Abnormal actin isoform expression has been reported in many cancers, which led us to hypothesize that it may serve as an early biomarker of cancer. We show an overview of the different actin isoforms and highlight mechanisms by which they may contribute to tumorigenicity. Furthermore, we suggest how the aberrant expression of actin subunits can confer cells with greater proliferation ability, increased migratory capability, and chemoresistance through incorporation into the normal cellular F-actin network and altered actin binding protein interaction. Studying this fundamental change that takes place within cancer cells can further our understanding of neoplastic transformation in multiple tissue types, which can ultimately aid in the early-detection, diagnosis and treatment of cancer.

摘要

肌动蛋白是一种关键的结构蛋白,构成细胞的细胞骨架,并在细胞分裂、迁移和囊泡运输等功能中发挥作用。它由六种不同的细胞类型特异性同工型组成:ACTA1、ACTA2、ACTB、ACTC1、ACTG1和ACTG2。许多癌症中都报道了肌动蛋白同工型表达异常,这使我们推测它可能作为癌症的早期生物标志物。我们概述了不同的肌动蛋白同工型,并强调了它们可能导致肿瘤发生的机制。此外,我们提出肌动蛋白亚基的异常表达如何通过并入正常细胞的F-肌动蛋白网络和改变肌动蛋白结合蛋白相互作用,赋予细胞更强的增殖能力、增加的迁移能力和化疗耐药性。研究癌细胞内发生的这一基本变化可以加深我们对多种组织类型肿瘤转化的理解,最终有助于癌症的早期检测、诊断和治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/5547da1c3d26/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/b3b4581457ce/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/4c9789d11842/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/2485adfa694f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/3cec14f905fa/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/5547da1c3d26/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/b3b4581457ce/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/4c9789d11842/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/2485adfa694f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/3cec14f905fa/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/862e/8008238/5547da1c3d26/gr4.jpg

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