Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion.

Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion.
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DOI:
10.1038/ncomms3268
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发表时间:
2013
影响因子:
16.6
通讯作者:
Lopez-Otin, Carlos
Lopez-Otin, Carlos
中科院分区:
综合性期刊1区
文献类型:
--
作者:
de la Rosa, Jorge;Freije, Jose M. P.;Cabanillas, Ruben;Osorio, Fernando G.;Fraga, Mario F.;Soledad Fernandez-Garcia, M.;Rad, Roland;Fanjul, Victor;Ugalde, Alejandro P.;Liang, Qi;Prosser, Haydn M.;Bradley, Allan;Cadinanos, Juan;Lopez-Otin, Carlos

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定义衰老与癌症之间的关系是一项至关重要但具有挑战性的任务。Zmpste24是一种在人类早衰症中突变的金属蛋白酶,参与核前层蛋白A的成熟,缺乏Zmpste24的小鼠重现了衰老的多种特征。然而,它们的寿命短,严重的细胞内在和细胞外在的改变限制了应用和解释的致癌协议。在这里,我们提出了Zmpste24嵌合小鼠,没有这些限制。Zmpste24嵌合体小鼠发育正常,并在整个生命周期中保持相似比例的Zmpste24缺陷(前核纤层蛋白A积累)和Zmpste24熟练(成熟核纤层蛋白A)细胞,揭示了细胞外在机制对早衰症的发展是突出的。此外,前层蛋白A的积累不损害肿瘤的发生和生长,但它降低了浸润性口腔癌的发病率。因此,ZMPSTE24的沉默降低了人癌细胞的侵袭性。我们的研究结果支持了基于细胞和全身疗法治疗早衰症的潜力,并突出了ZMPSTE24作为一个新的抗癌靶点。
Defining the relationship between ageing and cancer is a crucial but challenging task. Mice deficient in Zmpste24, a metalloproteinase mutated in human progeria and involved in nuclear prelamin A maturation, recapitulate multiple features of ageing. However, their short lifespan and serious cell-intrinsic and cell-extrinsic alterations restrict the application and interpretation of carcinogenesis protocols. Here we present Zmpste24 mosaic mice that lack these limitations. Zmpste24 mosaic mice develop normally and keep similar proportions of Zmpste24-deficient (prelamin A accumulating) and Zmpste24-proficient (mature lamin A containing) cells throughout life, revealing that cell-extrinsic mechanisms are preeminent for progeria development. Moreover, prelamin A accumulation does not impair tumour initiation and growth, but it decreases the incidence of infiltrating oral carcinomas. Accordingly, silencing of ZMPSTE24 reduces human cancer cell invasiveness. Our results support the potential of cell-based and systemic therapies for progeria and highlight ZMPSTE24 as a new anticancer target.
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