此前已經(jīng)有老鼠動(dòng)物研究證實(shí)端粒酶的缺失能拮抗癌變,。端粒耗損可以促進(jìn)癌癥早期基因組的不穩(wěn)定,，從而刺激引發(fā)腫瘤,，但同時(shí)也可以抑制腫瘤的發(fā)生,，促進(jìn)腫瘤細(xì)胞生長(zhǎng)停滯或死亡。
端粒酶-負(fù)責(zé)端粒的延長(zhǎng),。端粒酶的存在,，算是把 DNA 克隆機(jī)制的缺陷填補(bǔ)起來(lái)，藉由把端粒修復(fù)延長(zhǎng),，可以讓端粒不會(huì)因細(xì)胞分裂而有所損耗,，使得細(xì)胞分裂克隆的次數(shù)增加。
癌癥細(xì)胞系的端粒酶水平較低,，導(dǎo)致早期病變時(shí)的端粒缺失,，但隨后端粒酶會(huì)被激活。因此,，缺乏端粒酶的小鼠模型并為揭示端粒酶對(duì)細(xì)胞癌變的影響,。使用一種新的轉(zhuǎn)基因小鼠模型，Begus-Nahrmann研究人員證實(shí)了瞬態(tài)端粒酶功能障礙是導(dǎo)致腫瘤發(fā)生的一個(gè)強(qiáng)有力的刺激因子,。（生物谷：Bioon.com）
doi:10.1172/JCI63979
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Telomere stability and carcinogenesis: an off-again, on-again relationship
Jennifer J. Wanat and F. Brad Johnson
Previous studies in mice have demonstrated antagonistic effects of telomerase loss on carcinogenesis. Telomere attrition can promote genome instability, thereby stimulating initiation of early-stage cancers, but can also inhibit tumorigenesis by promoting permanent cell growth arrest or death. Human cancers likely develop in cell lineages with low levels of telomerase, leading to telomere losses in early lesions, followed by subsequent activation of telomerase. Mouse models constitutively lacking telomerase have thus not addressed how telomere losses within telomerase-proficient cells have an impact on carcinogenesis. Using a novel transgenic mouse model, Begus-Nahrmann et al. demonstrate in this issue of the JCI that transient telomere dysfunction in telomerase-proficient animals is a potent stimulus of tumor formation.
