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升级的表达层B受体增加细胞增殖和抑制基因组不稳定性:对细胞不朽化的影响

Atsuki En¹, Kentaro Takemoto¹, Yoshimi Yamakami¹

¹Graduate School of Nanobioscience, Yokohama City University, Japan.

The FEBS journal

|March 11, 2024

概括

细胞不朽化,逃避衰老,涉及到遗传改变. 在不朽化过程中,拉敏B受体 (LBR) 的表达增加,其敲击会诱导衰老,这表明LBR.

科学领域:

细胞和分子生物学细胞和分子生物学
癌症研究癌症研究
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

哺乳动物体细胞的分裂有限 (细胞衰老),但可以通过遗传变化实现无限的增殖 (细胞不朽).
瘤抑制基因失活 (例如,p53,RB) 是至关重要的,但不足以实现永生,这表明其他分子变化也参与其中.
衰老涉及改变的异性染色质组织,表明调节它的蛋白质,如拉胺B受体 (LBR),可能在不朽化中发挥作用.

研究的目的:

研究异色染色素调节剂,特别是LBR在细胞不朽化中的作用.
了解从衰老过渡到永生的基础上的分子机制.
确定涉及克服核扩散的新因素.

主要方法:

在人类永生细胞系中LBR表达的分析 (KMST-6,SUSM-1).
淘汰LBR,以评估其对细胞衰老和染色素的影响.
强制LBR表达在带有猿人病毒40大T抗原 (TAg) 的初级纤维细胞中,以评估对增殖和基因组不稳定性的影响.
调查LBR表达的变化,以响应TAG表达或p53敲击.

主要成果:

在永生细胞中,LBR表达被上调,在衰老细胞中被下调.
LBR倒置诱导了细胞衰老和改变了染色质配置.
强制LBR表达促进了细胞增殖,并抑制了TAg表达细胞中的基因组不稳定性.
TAg表达或p53敲击导致LBR表达的增加.

结论:

通过促进细胞增殖和抑制基因组不稳定性,LBR在细胞不朽化中发挥着至关重要的作用.
升级的LBR表达是p53/RB缺陷的细胞中不朽化的潜在机制.
LBR 是一个关键的调节者,它有助于从细胞衰老中逃脱.

关键词:

细胞不朽化细胞不朽化细胞衰老细胞衰老异性染色是一种异性染色.层B型受体的受体是什么

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