Research press release


Nature Cell Biology

Regulator limits tumour related cellular ageing


C-mycは健康な細胞を腫瘍細胞に転換させるのを助け、がんでは脱調節していることが多い。本来ならば、c-Mycの過剰発現はCdk2の活性化を引き起こし、細胞周期の進行を促進する。しかし、B Amariたちは、Cdk2遺伝子を欠くマウスの結合組織では、c-Mycの活性化が細胞老化につながることを見いだした。また、Cdk2を欠失するマウスのB細胞でc-Mycが発現すると、細胞老化が増進され、野生株の動物に比べてリンパ腫発症が遅れることもわかった。


The cell-cycle regulator Cdk2 suppresses the initiation of a cellular ageing process that is seen as a barrier against tumour progression. The finding, online this week in Nature Cell Biology, suggests that inhibiting Cdk2 may be a useful therapeutic tool for halting the progression of certain types of tumours.

C-myc ― a gene which helps to turn healthy cells into tumour cells ― is frequently deregulated in cancer. Overexpression of c-Myc normally causes activation of Cdk2 and promotes cell-cycle progression. However, Bruno Amati and colleagues find that in connective tissue of mice lacking the Cdk2 gene, c-Myc activation leads to cellular ageing. They also note that when c-Myc was expressed in B-cells, increased cellular ageing and delayed onset of lymphoma was observed in animals lacking Cdk2 when compared to wild-type animals. The team report that inhibition of Cdk2 causes ageing in Myc-overexpressing cells, while neither Cdk2 inhibition or Myc overexpression alone had this effect.

doi: 10.1038/ncb2004


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