Karyoptosis as a novel type of UVB-induced regulated cell death.

IF 3.6 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Free Radical Research Pub Date : 2024-11-01 Epub Date: 2024-12-03 DOI:10.1080/10715762.2024.2433986
Weidong Chen, Jiin Byun, Han Chang Kang, Hye Suk Lee, Joo Young Lee, Young Jik Kwon, Yong-Yeon Cho
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引用次数: 0

Abstract

Karyoptosis is a type of regulated cell death (RCD) characterized by explosive nuclear rupture caused by a loss of nuclear membrane integrity, resulting in the release of genomic DNA and other nuclear components into the cytosol and extracellular environment. The mechanism underlying karyoptosis involves a delicate balance between the following forces: the expansion force exerted by the tightly packed DNA in the nucleus, the resistance provided by the nuclear lamina at the inner nuclear membrane (INM), and the tensile force from the cytoskeleton that helps position the nucleus at the center of the cytoplasm, allowing it to remain maximally expanded. In addition, CREB3, a type II integral membrane protein with DNA-binding ability, tethers chromatin to the INM, providing a tightening force through chromatin interactions that prevent nuclear membrane rupture. UVB radiation can trigger this process, inducing CREB3-FL cleavage and producing CREB3-CF. Therefore, UVB acts as an intrinsic factor in the induction of karyoptosis. Importantly, biochemical analysis of RCD markers shows that karyoptosis is distinct from other forms of cell death, such as apoptosis, autophagy, necroptosis, and pyroptosis. This review explores the mechanisms involved in maintaining nuclear membrane integrity and the role of CREB3 in triggering karyoptosis and provides brief suggestions on the potential implications for targeting cancer cells.

核衰是一种新型的uvb诱导的细胞死亡。
核衰是一种受调控的细胞死亡(RCD),其特征是核膜完整性丧失引起的爆炸性核破裂,导致基因组DNA和其他核成分释放到细胞质和细胞外环境中。核凋亡的机制涉及以下力量之间的微妙平衡:细胞核中紧密排列的DNA施加的膨胀力,核膜(INM)上的核层提供的阻力,以及来自细胞骨架的张力,这有助于将细胞核定位在细胞质的中心,使其保持最大程度的膨胀。此外,CREB3是一种具有dna结合能力的II型完整膜蛋白,它将染色质系在INM上,通过染色质相互作用提供紧固力,防止核膜破裂。UVB辐射可以触发这一过程,诱导CREB3-FL裂解,生成CREB3-CF。因此,UVB是诱导核衰的内在因素。重要的是,RCD标记物的生化分析表明,核凋亡不同于其他形式的细胞死亡,如凋亡、自噬、坏死坏死和焦亡。本文探讨了维持核膜完整性的机制以及CREB3在触发核衰中的作用,并就其靶向癌细胞的潜在意义提出了简要建议。
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
Free Radical Research
Free Radical Research 生物-生化与分子生物学
CiteScore
6.70
自引率
0.00%
发文量
47
审稿时长
3 months
期刊介绍: Free Radical Research publishes high-quality research papers, hypotheses and reviews in free radicals and other reactive species in biological, clinical, environmental and other systems; redox signalling; antioxidants, including diet-derived antioxidants and other relevant aspects of human nutrition; and oxidative damage, mechanisms and measurement.
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