癌症生物学中早期应激反应的自我组织

J. Erenpreisa, K. Salmina, N. Vainshelbaum, I. Inashkina, T. Freivalds
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摘要

在癌症中,AP-1(FOS/JUN)的早期应激反应得到了 c-Myc 上调的支持,并参与了细胞命运的改变和对恶劣环境的适应。综述显示了这种反应的双相特性,其负反馈通常持续几个小时,这是基因组自组织临界调控的一个特征。它包括中心粒周围异染色质群的快速分裂、活性染色质的开放以及大规模的转录加速波。植物地层学分析显示,AP-1 基因是在约 500 Mya 的寒武纪大爆发中进化而来的,它整合了生殖的蛋白质相互作用网络,包括与细胞因子和免疫途径、性别决定、卵母细胞成熟和胚胎干性交织在一起的原胎盘。在对多柔比星耐药的乳腺癌细胞系中发现,这种反应的峰值是由 AP-1 和 IL-1β 导致的细胞加速衰老的一部分。侵袭性癌症对治疗的适应性可以用进化过程中出现的保护生殖的应激反应来解释
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Self-organisation of early stress response in the biology of cancer
The early stress response by AP-1 (FOS/JUN), supported by upregulation of c-Myc and involved in cell-fate changes and adaptation to hostile environments, is increased in cancer. The review shows the biphasic character of this response with negative feed-back typically lasting a few hours as a feature of the genome regulation by self-organising criticality. It involves  rapid splitting of the pericentromeric heterochromatin clusters, opening of the active chromatin, and a massive transcription acceleration wave. Phylostratigraphic analysis revealed that AP-1 genes evolved in the Cambrian explosion ~500 Mya integrating the protein interaction networks of reproduction including proto-placenta intertwined with cytokine and immunity pathways, sex determination, oocyte maturation, and embryonal stemness. The peak  of this response as part of accelerated cell senescence led by AP-1 and IL-1β was found in breast cancer cell-line resistant to doxorubicin. Adaptability of aggressive cancer to treatments can be explained by emergent stress response evolutionarily protecting reproduction
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