Cell Rep:揭开癌细胞逃逸存活的又一大谜题

2014-08-11 佚名 生物谷

近日,来自明尼苏达大学等处的科学家们通过研究揭开了癌症研究领域的一个谜题,即当染色体老化时促使得恶性细胞绕过细胞正常死亡过程的机制,相关研究刊登于国际杂志Cell Reports上。 长期以来科学家们熟知当细胞不断地重复分裂时往往会引发染色体的缺陷,而染色体缺陷则和癌症发病直接相关,如今研究人员发人类细胞需要一种特殊的基因来在众多缺陷环境中得以存活。研究者Hendrickson教授表示,我们鉴别

近日,来自明尼苏达大学等处的科学家们通过研究揭开了癌症研究领域的一个谜题,即当染色体老化时促使得恶性细胞绕过细胞正常死亡过程的机制,相关研究刊登于国际杂志Cell Reports上。

长期以来科学家们熟知当细胞不断地重复分裂时往往会引发染色体的缺陷,而染色体缺陷则和癌症发病直接相关,如今研究人员发人类细胞需要一种特殊的基因来在众多缺陷环境中得以存活。研究者Hendrickson教授表示,我们鉴别出了一种新型基因,其可以调节细胞使其癌变或者正常生存

随着细胞分裂过程中端粒的分离,染色体就会对彼此的吸附作用变得更加敏感;在正常细胞中,染色体的粘性是一种死亡信号,该信号可以帮助清除机体中不健全的细胞,然而恶性发育的细胞有时候就会躲避过此信号的作用。文章中研究人员发现了一种可以使得衰老细胞躲避死亡的必要组分,利用复杂的基因靶向技术,研究人员就可以将人类细胞中的特殊基因失活,并且研究其对端粒融合的影响,研究者们发现,当基因Ligase 3处于活化状态时衰老细胞就可以躲过死亡一劫。

Baird博士表示,在许多人类癌症中都发现了细胞中端粒的功能障碍,而在此前研究中我们发现端粒变短或可帮助预测人类的疾病,比如癌症的发生等;而本文中基因Ligase 3的发现为解析癌症的发生又增加了新的依据。

后期还需要进行更多的研究,尤其是基因Ligase 3的发现,该基因还依赖于另一种关键的DNA修复基因p53的帮助,p53在许多人类癌症中都处于突变的状态,研究者们将去研究基因p53和Ligase 3的相互作用机制,来开发新型的癌症靶向协同疗法帮助治疗人类癌症。

原始出处:

Rhiannon E. Jones3, Sehyun Oh3, Julia W. Grimstead3, Jacob Zimbric, Laureline Roger, Nicole H. Heppel, Kevin E. Ashelford, Kate Liddiard, Eric A. Hendrickson4, Duncan M. Baird4.Escape from Telomere-Driven Crisis Is DNA Ligase III Dependent.Cell Rep doi:10.1016/j.celrep.2014.07.007

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    2015-02-27 维他命
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    2014-08-13 yxch36