miR-22 represses cancer progression by inducing cellular senescence

Dan Xu(Hiroshima University), Fumitaka Takeshita, Yumiko Hino(Hiroshima University), Saori Fukunaga(Hiroshima University), Yasusei Kudo(Hiroshima University), Aya Tamaki(Hiroshima University), Junko Matsunaga(Hiroshima University), Ryou‐u Takahashi, Takashi Takata(Hiroshima University), Akira Shimamoto(Hiroshima University), Takahiro Ochiya, Hidetoshi Tahara(Hiroshima University)
The Journal of Cell Biology
April 18, 2011
Cited by 289Open Access
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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.


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