美國(guó)科學(xué)家近日研究發(fā)現(xiàn)，秀麗隱桿線(xiàn)蟲(chóng)（C. elegans）體內(nèi)含有多種能夠同時(shí)減緩老化和抑制腫瘤細(xì)胞生長(zhǎng)的基因,。由于C. elegans的多種基因與人類(lèi)的相似,，所以此次發(fā)現(xiàn)意味著,，也許有一天科學(xué)家將開(kāi)發(fā)出能夠延長(zhǎng)壽命并避免癌癥的藥物。相關(guān)論文10月14日在線(xiàn)發(fā)表于《自然－遺傳學(xué)》上,。
該項(xiàng)研究由美國(guó)加州大學(xué)舊金山分校的Cynthia Kenyon教授領(lǐng)導(dǎo)完成,。她曾于1993年發(fā)現(xiàn)，改變一個(gè)單獨(dú)的daf-2基因能夠使C. elegans的壽命延長(zhǎng)一倍,。這表明,，壽命由基因調(diào)控，并且可以改變,。
daf-2基因用于編碼胰島素受體和一個(gè)能促進(jìn)生長(zhǎng)的類(lèi)胰島素蛋白,，它會(huì)影響daf-16基因生成轉(zhuǎn)錄因子以決定其它幾百種基因開(kāi)啟的時(shí)間和地點(diǎn)。最新研究的目的在于找出由daf-16調(diào)控的特定基因,，這些基因會(huì)影響癌癥和壽命,。
研究小組應(yīng)用多種技術(shù)，包括RNA干涉等,，從734種基因中鑒別出了29種能夠影響腫瘤細(xì)胞生長(zhǎng)的基因,。其中，促進(jìn)者和抑制者大約各一半,。另外,，這些基因中大約有一半也能夠影響體內(nèi)并無(wú)腫瘤動(dòng)物的壽命。
Kenyon表示,，這一發(fā)現(xiàn)讓人非常激動(dòng),。之前很多人認(rèn)為，任何能夠延緩老化的機(jī)制必將刺激腫瘤的生長(zhǎng),，但是最新研究卻發(fā)現(xiàn)了很多能夠同時(shí)延緩老化和抑制腫瘤生長(zhǎng)的基因,。也許將來(lái)更深入的研究能夠幫助人們保持年輕并遠(yuǎn)離癌癥。（科學(xué)網(wǎng) 梅進(jìn)/編譯）
原始出處：
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: [email protected]
