Oxidative stress induces cortical stiffening and cytoskeletal remodelling in pre-apoptotic cancer cells.

IF 3 Q2 CELL BIOLOGY

Cell Stress Pub Date : 2025-08-07 eCollection Date: 2025-01-01 DOI:10.15698/cst2025.08.310

Aiman Jalmukhambetova, Aidana Baltabekova, Aizhan Tolebay, Nargiz Rakhimgerey, Ferdinand Molnár, Tri Thanh Pham, Agata N Burska, Dos D Sarbassov

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引用次数: 0

Abstract

An imbalanced production of reactive oxygen species (ROS) is linked to various aspects of cancer development, including cytoskeletal remodelling. However, the relationship between ROS, actin and cellular stiffness remains controversial. Here, we show that oxidative stress increases cortical stiffness in pre-apoptotic colon and pancreatic cancer cells via localized F-actin polymerization in the apical cortex - independent of changes in total F-actin levels. Using atomic force microscopy and flow cytometry, we demonstrate this effect across multiple ROS inducers: the combination of arsenic trioxide and D-enantiomer of vitamin C, hydrogen peroxide, and rotenone. These findings explain previously debated relationships on how ROS influence actin organization, which may affect cellular stiffness. By separating total from cortical actin effects, our study reveals a redox-sensitive mechanism that governs cytoskeletal remodelling and may impair cancer cell migration.

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氧化应激诱导凋亡前癌细胞的皮质硬化和细胞骨架重塑。

活性氧（ROS）的不平衡产生与癌症发展的各个方面有关，包括细胞骨架重塑。然而，活性氧、肌动蛋白和细胞硬度之间的关系仍然存在争议。在这里，我们发现氧化应激通过在顶端皮层的局部f -肌动蛋白聚合增加了凋亡前结肠癌和胰腺癌细胞的皮质硬度，而不依赖于总f -肌动蛋白水平的变化。利用原子力显微镜和流式细胞术，我们证明了这种效应跨越多种ROS诱导剂：三氧化二砷和维生素C的d -对映体、过氧化氢和鱼藤酮的组合。这些发现解释了之前关于ROS如何影响肌动蛋白组织的争论关系，这可能会影响细胞硬度。通过分离总肌动蛋白和皮质肌动蛋白的作用，我们的研究揭示了一种氧化还原敏感机制，它控制着细胞骨架的重塑，并可能损害癌细胞的迁移。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Stress Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (miscellaneous)

CiteScore

13.50

自引率

0.00%

发文量

审稿时长

15 weeks

期刊介绍： Cell Stress is an open-access, peer-reviewed journal that is dedicated to publishing highly relevant research in the field of cellular pathology. The journal focuses on advancing our understanding of the molecular, mechanistic, phenotypic, and other critical aspects that underpin cellular dysfunction and disease. It specifically aims to foster cell biology research that is applicable to a range of significant human diseases, including neurodegenerative disorders, myopathies, mitochondriopathies, infectious diseases, cancer, and pathological aging. The scope of Cell Stress is broad, welcoming submissions that represent a spectrum of research from fundamental to translational and clinical studies. The journal is a valuable resource for scientists, educators, and policymakers worldwide, as well as for any individual with an interest in cellular pathology. It serves as a platform for the dissemination of research findings that are instrumental in the investigation, classification, diagnosis, and therapeutic management of major diseases. By being open-access, Cell Stress ensures that its content is freely available to a global audience, thereby promoting international scientific collaboration and accelerating the exchange of knowledge within the research community.