@article{02119c0b4bc14305b84abdc4dc9b87b0,
title = "Posttranscriptional regulation of miRNAs in the DNA damage response",
abstract = "DNA damage response is an elaborate process in which cells react to external or internal DNA damaging stress. An extensive network of signaling molecules, complexes and pathways has been identified in the DNA damage response. Emerging evidence indicates that microRNAs (miRNAs) play essential roles in the DNA damage and repair pathways. While much effort has been to predict in silico and verify miRNA target genes, little is known about how miRNAs themselves respond to DNA damage. Here we discuss recent studies showing whether and how miRNAs are regulated in the DNA damage response. MiRNA expression involves transcription of miRNA genes and maturation of the primary transcripts. Therefore, miRNA levels might be regulated in both transcription dependent and independent manners. While the DNA damage response is known to protect against tumorigenesis in vivo, a deficient response could contribute to tumorigenesis through miRNAs.",
keywords = "DNA damage response, DNA repair, KSRP, MicroRNA expression, Processing",
author = "Xinna Zhang and Xiongbin Lu",
note = "Funding Information: Although mature miRNAs are non-coding small RNAs that differ from mRNAsand other types of RNAs, the primarytranscripts of miRNAs (that are pri-miRNAs) share similar characteristics of mRNAs. Therefore, certain pathways may Recent reports suggest that miRNA expression is deregulated in human cancer. There appears to be a global repression of miRNA expression in cancer tissues and cells.26 Dicer mutation or dysregulation contributes to reduced miRNA expressions. Dicer functions as a haplo-insufficient tumor suppressor in vivo.27,28 Impaired miRNA processing accelerates tumor formation and increased tumor invasion. While Dicer knockout mice are embryonic lethal, conditional deletion of Dicer1 in a K-Ras-induced lung cancer model markedly enhanced tumor progression.28 Lanbertz The authors thank their lab members and colleagues for helpful discussions. X.L. is supported by grants from the National Institutes of Health (R01CA136549, R03CA142605), the American Cancer Society (119135-RSG-10-185-01-TBE), and The University of Texas MD Anderson Cancer Center (New Faculty Start-up Fund).",
year = "2011",
doi = "10.4161/rna.8.6.17337",
language = "English (US)",
volume = "8",
journal = "RNA Biology",
issn = "1547-6286",
publisher = "Landes Bioscience",
number = "6",
}