美国科学家近日研究发现，秀丽隐杆线虫（C. elegans）体内含有多种能够同时减缓老化和抑制肿瘤细胞生长的基因。由于C. elegans的多种基因与人类的相似，所以此次发现意味着，也许有一天科学家将开发出能够延长寿命并避免癌症的药物。相关论文10月14日在线发表于《自然－遗传学》上。
该项研究由美国加州大学旧金山分校的Cynthia Kenyon教授领导完成。她曾于1993年发现，改变一个单独的daf-2基因能够使C. elegans的寿命延长一倍。这表明，寿命由基因调控，并且可以改变。
daf-2基因用于编码胰岛素受体和一个能促进生长的类胰岛素蛋白，它会影响daf-16基因生成转录因子以决定其它几百种基因开启的时间和地点。最新研究的目的在于找出由daf-16调控的特定基因，这些基因会影响癌症和寿命。
研究小组应用多种技术，包括RNA干涉等，从734种基因中鉴别出了29种能够影响肿瘤细胞生长的基因。其中，促进者和抑制者大约各一半。另外，这些基因中大约有一半也能够影响体内并无肿瘤动物的寿命。
Kenyon表示，这一发现让人非常激动。之前很多人认为，任何能够延缓老化的机制必将刺激肿瘤的生长，但是最新研究却发现了很多能够同时延缓老化和抑制肿瘤生长的基因。也许将来更深入的研究能够帮助人们保持年轻并远离癌症。（科学网 梅进/编译）
原始出处：
Nature Genetics
Published online: 14 October 2007 | doi:10.1038/ng.2007.1
DAF-16/FOXO targets genes that regulate tumor growth in Caenorhabditis elegans
Julie Pinkston-Gosse1 & Cynthia Kenyon1
Cancer is an age-related disease, and inhibiting insulin/insulin-like growth factor 1 (IGF-1) signaling extends lifespan and increases tumor resistance in C. elegans and mammals. To investigate how the insulin/IGF-1 pathway couples these two processes, we analyzed putative transcriptional targets of the C. elegans FOXO transcription factor DAF-16, which promotes both longevity and tumor resistance. Twenty-nine of 734 genes tested influenced germline-tumor cell proliferation or p53-dependent apoptosis. About half of these genes also affected normal aging, thereby linking these two processes mechanistically. Many of these 29 genes are orthologs of known human tumor suppressors or oncogenes, suggesting that others may be as well. Our findings implicate nuclear-pore modification in p53-dependent cell death, because inhibiting nuclear-pore genes that are upregulated by DAF-16 blocks p53-dependent cell death in the tumor, but not normal, p53-independent, germline cell death.
Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California 94158, USA.
Correspondence to: Cynthia Kenyon1 e-mail: ckenyon@biochem.ucsf.edu
