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Accepted Preprint first posted online on 24 September 2009

Endocrine-Related Cancer 2010;17:F19.

DOI: 10.1677/ERC-09-0184
Copyright © 2009 by the Society for Endocrinology.
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REVIEW

The role of Let-7 in cell differentiation and cancer

Benjamin Boyerinas, Sun-Mi Park, Annika Hau, Andrea E Murmann and Marcus E Peter

B Boyerinas, The Ben May Department for Cancer Research, The University of Chicago, Chicago, United States
S Park, The Ben May Department for Cancer Research, The University of Chicago, Chicago, United States
A Hau, The Ben May Department for Cancer Research, The University of Chicago, Chicago, United States
A Murmann, The Ben May Department for Cancer Research, The University of Chicago, Chicago, United States
M Peter, The Ben May Department for Cancer Research, The University of Chicago, Chicago, United Kingdom

Correspondence: Marcus E Peter, Email: mpeter{at}uchicago.edu

Abstract

MicroRNAs (miRNAs) are small non-coding RNAs capable of regulating gene expression at the translational level. Current evidence suggests that a significant portion of the human genome is regulated by miRNAs, and many reports have demonstrated that miRNA expression is deregulated in human cancer. The let-7 family of miRNAs, first discovered in C. elegans, is functionally conserved from worms to humans. The human let-7 family contains 13 members located on 9 different chromosomes, and many human cancers have deregulated let-7 expression. A growing body of evidence suggests that restoration of let-7 expression may be a useful therapeutic option in cancers where its expression has been lost. In this review, we discuss the role of let-7 in normal development and differentiation and provide an overview of the relationship between deregulated let-7 expression and tumorigenesis. The regulation of let-7 expression, cancer-relevant let-7 targets, and the relationship between let-7 and drug sensitivity are highlighted.




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A. Fusco
MicroRNAs: a great challenge for the diagnosis and therapy of endocrine cancers
Endocr. Relat. Cancer, January 29, 2010; 17(1): E3 - E4.
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