miR-107 promotes tumor progression by targeting the let-7 microRNA in mice and humans

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/16731

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题名:	miR-107 promotes tumor progression by targeting the let-7 microRNA in mice and humans
作者:	蘇振良;Su, Jen-Liang;Kuo-Tai Hua,;Chiung-Nien Chen,;Kuo, Tsang-Chih;Chang, King-Jen;Hsiao, Michael;Chang, Yi-Wen
贡献者:	生物科技學系
关键词:	RNA;COCARCINOGENS;CANCER invasiveness;GENE expression;CARCINOGENESIS
日期:	2011-09
上传时间:	2012-11-23 09:16:23 (UTC+0)
摘要:	MicroRNAs (miRNAs) influence many biological processes, including cancer. They do so by posttranscriptionally repressing target mRNAs to which they have sequence complementarity. Although it has been postulated that miRNAs can regulate other miRNAs, this has never been shown experimentally to our knowledge. Here, we demonstrate that miR-107 negatively regulates the tumor suppressor miRNA let-7 via a direct interaction. miR-107 was found to be highly expressed in malignant tissue from patients with advanced breast cancer, and its expression was inversely correlated with let-7 expression in tumors and in cancer cell lines. Ectopic expression of miR-107 in human cancer cell lines led to destabilization of mature let-7, increased expression of let-7 targets, and increased malignant phenotypes. In contrast, depletion of endogenous miR-107 dramatically increased the stability of mature let-7 and led to downregulation of let-7 targets. Accordingly, miR-107 expression increased the tumorigenic and metastatic potential of a human breast cancer cell line in mice via inhibition of let-7 and upregulation of let-7 targets. By mutating individual sites within miR-107 and let-7, we found that miR-107 directly interacts with let-7 and that the internal loop of the let-7/miR-107 duplex is critical for repression of let-7 expression. Altogether, we have identified an oncogenic role for miR-107 and provide evidence of a transregulational interaction among miRNAs in human cancer development.
關聯:	JOURNAL OF CLINICAL INVESTIGATION
显示于类别:	[生物科技學系] 期刊論文

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