Regression of murine lung tumors by the let-7 microRNA

被引：376

作者：

Trang, P. ^{[2
,3
]}

Medina, P. P. ^{[2
]}

Wiggins, J. F. ^{[1
]}

Ruffino, L. ^{[1
]}

Kelnar, K. ^{[1
]}

Omotola, M. ^{[1
]}

Homer, R. ^{[4
,5
]}

Brown, D. ^{[1
]}

Bader, A. G. ^{[1
]}

Weidhaas, J. B. ^{[3
]}

Slack, F. J. ^{[2
]}

机构：

[1] Mirna Therapeut Inc, Austin, TX USA

[2] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT USA

[3] Yale Univ, Sch Med, Dept Therapeut Radiol, New Haven, CT 06510 USA

[4] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA

[5] VA Connecticut Healthcare Syst, Dept Pathol & Lab Med Serv, West Haven, CT USA

来源：

ONCOGENE | 2010年 / 29卷 / 11期

关键词：

let-7; microRNAs; lung cancer; K-ras; MOUSE MODELS; K-RAS; CANCER; EXPRESSION; INHIBITION; FAMILY; GROWTH; CELLS; SIRNA; HMGA2;

D O I：

10.1038/onc.2009.445

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

MicroRNAs (miRNAs) have recently emerged as an important new class of cellular regulators that control various cellular processes and are implicated in human diseases, including cancer. Here, we show that loss of let-7 function enhances lung tumor formation in vivo, strongly supporting the hypothesis that let-7 is a tumor suppressor. Moreover, we report that exogenous delivery of let-7 to established tumors in mouse models of non-small-cell lung cancer (NSCLC) significantly reduces the tumor burden. These results demonstrate the therapeutic potential of let-7 in NSCLC and point to miRNA replacement therapy as a promising approach in cancer treatment. Oncogene (2010) 29, 1580-1587; doi:10.1038/onc.2009.445; published online 7 December 2009

引用

页码：1580 / 1587

页数：8

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