日本广岛大学细胞分子生物学教授田原荣俊宣布，他们的研究小组研究发现，一种存在于细胞和血液中、被称为“微型核糖核酸（miR22）”的物质，可以使乳腺癌和宫颈癌的癌细胞衰老，从而具有抑制癌细胞增殖和转移的功能。这一研究结果刊登在4月18日出版的美国科学杂志上。
一般认为微型RNA与调节细胞增殖、细胞分化等各种生物现象有关，正常细胞老化停止分裂时微型RNA会增加。
研究小组对不发生老化而进化为癌症的细胞中miR22的减少进行了研究。在培养的乳腺癌和宫颈癌的癌细胞中加入miR22，癌细胞老化程度加重，分裂被抑制。在小鼠的试验中同样发现了乳腺癌的转移被控制。
田原教授认为，细胞老化是生物体防止癌症发生的自身防御机制。细胞内微型RNA减少会阻碍细胞老化，从而促使癌细胞发生，而加入miR22之后，机体内老化程序恢复，进而抑制了癌细胞的繁殖。
田原教授说，微型RNA是生物体内制造的一种物质，与目前的抗癌制剂相比具有副作用小的优势，有望用来研制下一代抗癌药物。（生物谷Bioon.com）
生物谷推荐原文出处：
JCB doi: 10.1083/jcb.201010100
miR-22 represses cancer progression by inducing cellular senescence
Dan Xu1, Fumitaka Takeshita3, Yumiko Hino1, Saori Fukunaga1, Yasusei Kudo2, Aya Tamaki1, Junko Matsunaga1, Ryou-u Takahashi3, Takashi Takata2, Akira Shimamoto1, Takahiro Ochiya3, and Hidetoshi Tahara1
Abstract
Cellular senescence acts as a barrier to cancer progression, and microRNAs (miRNAs) are thought to be potential senescence regulators. However, whether senescence-associated miRNAs (SA-miRNAs) contribute to tumor suppression remains unknown. Here, we report that miR-22, a novel SA-miRNA, has an impact on tumorigenesis. miR-22 is up-regulated in human senescent fibroblasts and epithelial cells but down-regulated in various cancer cell lines. miR-22 overexpression induces growth suppression and acquisition of a senescent phenotype in human normal and cancer cells. miR-22 knockdown in presenescent fibroblasts decreased cell size, and cells became more compact. miR-22–induced senescence also decreases cell motility and inhibits cell invasion in vitro. Synthetic miR-22 delivery suppresses tumor growth and metastasis in vivo by inducing cellular senescence in a mouse model of breast carcinoma. We confirmed that CDK6, SIRT1, and Sp1, genes involved in the senescence program, are direct targets of miR-22. Our study provides the first evidence that miR-22 restores the cellular senescence program in cancer cells and acts as a tumor suppressor.
