Gibieža Paulius, Petrikaitė Vilma
Laboratory of Drug Targets Histopathology, Institute of Cardiology, Lithuanian University of Health Sciences Kaunas, LT-50162, Lithuania.
Am J Cancer Res. 2021 Sep 15;11(9):4050-4069. eCollection 2021.
Actin is the most abundant protein in almost all the eukaryotic cells. Actin amino acid sequences are highly conserved and have not changed a lot during the progress of evolution, varying by no more than 20% in the completely different species, such as humans and algae. The network of actin filaments plays a crucial role in regulating cells' cytoskeleton that needs to undergo dynamic tuning and structural changes in order for various functional processes, such as cell motility, migration, adhesion, polarity establishment, cell growth and cell division, to take place in live cells. Owing to its fundamental role in the cell, actin is a prominent regulator of cell division, a process, whose success directly depends on morphological changes of actin cytoskeleton and correct segregation of duplicated chromosomes. Disorganization of actin framework during the last stage of cell division, known as cytokinesis, can lead to multinucleation and formation of polyploidy in post-mitotic cells, eventually developing into cancer. In this review, we will cover the principles of actin regulation during cell division and discuss how the control of actin dynamics is altered during the state of malignancy.
肌动蛋白是几乎所有真核细胞中含量最丰富的蛋白质。肌动蛋白的氨基酸序列高度保守，在进化过程中变化不大，在完全不同的物种（如人类和藻类）中差异不超过20%。肌动蛋白丝网络在调节细胞的细胞骨架中起着关键作用，细胞骨架需要进行动态调整和结构变化，以便在活细胞中发生各种功能过程，如细胞运动、迁移、黏附、极性建立、细胞生长和细胞分裂。由于其在细胞中的基本作用，肌动蛋白是细胞分裂的重要调节因子，细胞分裂过程的成功直接取决于肌动蛋白细胞骨架的形态变化和复制染色体的正确分离。在细胞分裂的最后阶段，即胞质分裂过程中，肌动蛋白框架的紊乱会导致有丝分裂后细胞出现多核化和多倍体形成，最终发展成癌症。在这篇综述中，我们将阐述细胞分裂过程中肌动蛋白调节的原理，并讨论在恶性状态下肌动蛋白动力学的控制是如何改变的。
