癌症的产生可能是由于细胞衰老导致？

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" L2 r, g% e3 J/ y. \【研究】癌症的产生可能是由于细胞衰老导致？& |: m! X& U  O! p' {6 x
2013-11-27 生物谷
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, p2 r! }7 i8 i' Y. Y近期发表在Nature Cell Biology杂志上的文章称，癌症的产生可能是由于细胞衰老导致的。0 ~7 x: E$ K& t& U1 A8 Y
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英国格拉斯哥的Beatson癌症研究中心科学家发现有些癌症并不是是完全由于遗传物质破坏造成的，而是由于衰老细胞绕过了阻止其生长开关导致的。
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- M% E' T7 z. u$ u4 Q科学家采用人类细胞培养技术，发现几近寿命的细胞调控DNA能力降低，即DNA甲基化能力。而该DNA甲基化模式与癌细胞中的模式类似。DNA甲基化能够控制基因开关，在控制细胞行为中有重要作用。
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该文章的作者之一Peter Adams博士称，衰老是多数癌症最大的单一风险因子，但是我们对衰老和癌症的关系却知之甚少。本研究中，我们发现衰老细胞与正常细胞有明显的不同。我们发现当细胞条件改变或细胞太过衰老不能控制自己的时候就会引起细胞癌变。: e( }* @1 m- Z

7 B3 R3 C& y! `+ g英国癌症研究专家Kat Arney博士称，在细胞癌变的研究中，我们仅仅是刚起步，该研究表明衰老细胞更容易癌变，加深了我们对该问题的理解。该基础研究对我们开发新的治疗方法治疗癌症提供了新的依据。（生物谷Bioon.com）* v( F9 s5 \! A- b$ v
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Senescent cells harbour features of the cancer epigenome
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Cruickshanks HA, McBryan T, Nelson DM, Vanderkraats ND, Shah PP, van Tuyn J, Singh Rai T, Brock C, Donahue G, Dunican DS, Drotar ME, Meehan RR, Edwards JR, Berger SL, Adams PD.
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. |1 F$ W% S8 A0 H2 jAltered DNA methylation and associated destabilization of genome integrity and function is a hallmark of cancer. Replicative senescence is a tumour suppressor process that imposes a limit on the proliferative potential of normal cells that all cancer cells must bypass. Here we show by whole-genome single-nucleotide bisulfite sequencing that replicative senescent human cells exhibit widespread DNA hypomethylation and focal hypermethylation. Hypomethylation occurs preferentially at gene-poor, late-replicating, lamin-associated domains and is linked to mislocalization of the maintenance DNA methyltransferase (DNMT1) in cells approaching senescence. Low-level gains of methylation are enriched in CpG islands, including at genes whose methylation and silencing is thought to promote cancer. Gains and losses of methylation in replicative senescence are thus qualitatively similar to those in cancer, and this 'reprogrammed' methylation landscape is largely retained when cells bypass senescence. Consequently, the DNA methylome of senescent cells might promote malignancy, if these cells escape the proliferative barrier.
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