Dicer is regulated by cellular stresses and interferons

被引：160

作者：

Wiesen, Jennifer L. ^{[1
]}

Tomasi, Thomas B. ^{[1
,2
]}

机构：

[1] Roswell Pk Canc Inst, Mol Med Lab, Dept Immunol, Buffalo, NY 14263 USA

[2] SUNY Buffalo, Dept Med & Microbiol & Immunol, Sch Med & Biomed Sci, Buffalo, NY 14214 USA

来源：

MOLECULAR IMMUNOLOGY | 2009年 / 46卷 / 06期

基金：

美国国家卫生研究院;

关键词：

RNAi; MicroRNA; Dicer; Stress; Interferon; HISTONE DEACETYLASE INHIBITOR; TUMOR-CELLS; INDUCED APOPTOSIS; GENE-EXPRESSION; MICRORNAS; RNA; ACETYLATION; ACTIVATION; REPRESSION; INDUCTION;

D O I：

10.1016/j.molimm.2008.11.012

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：

The generation of microRNAs is dependent on the RNase III enzyme Dicer, the levels of which vary in different normal cells and in disease states. We demonstrate that Dicer protein expression in JAR trophoblast cells, and several other cell types, was inhibited by multiple stresses including reactive oxygen species, phorbol esters and the Ras oncogene. Additionally, double-stranded RNA and Type I interferons repress Dicer protein in contrast to IFN-gamma which induces Dicer. The effects of stresses and interferons are primarily post-transcriptional. The findings suggest that Dicer is a stress response component and identifies interferons as potentially important regulators of Dicer expression. (C) 2008 Elsevier Ltd. All rights reserved.

引用

页码：1222 / 1228

页数：7

共 42 条

[31]

Rosato RR, 2003, CANCER RES, V63, P3637

[32] The histone deacetylase inhibitor and chemotherapeutic agent suberoylanilide hydroxamic acid (SAHA) induces a cell-death pathway characterized by cleavage of Bid and production of reactive oxygen species [J].

Ruefli, AA ;

Ausserlechner, MJ ;

Bernhard, D ;

Sutton, VR ;

Tainton, KM ;

Kofler, R ;

Smyth, MJ ;

Johnstone, RW .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (19) :10833-10838

[33] Extensive variation in the 5′-UTR of dicer mRNAs influences translational efficiency [J].

Singh, S ;

Bevan, SC ;

Patil, K ;

Newton, DC ;

Marsden, PA .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2005, 335 (03) :643-650

[34] Type I interferons in host defense [J].

Stetson, Daniel B. ;

Medzhitov, Ruslan .

IMMUNITY, 2006, 25 (03) :373-381

[35] Cellular internal ribosome entry segments:: structures, trans-acting factors and regulation of gene expression [J].

Stoneley, M ;

Willis, AE .

ONCOGENE, 2004, 23 (18) :3200-3207

[36] Extensive post-transcriptional regulation of microRNAs and its implications for cancer [J].

Thomson, J. Michael ;

Newman, Martin ;

Parker, Joel S. ;

Morin-Kensicki, Elizabeth M. ;

Wright, Tricia ;

Hammond, Scott M. .

GENES & DEVELOPMENT, 2006, 20 (16) :2202-2207

[37] Interferon α-induced apoptosis in tumor cells is mediated through the phosphoinositide 3-kinase/mammalian target of rapamycin signaling pathway [J].

Thyrell, L ;

Hjortsberg, L ;

Arulampalam, V ;

Panaretakis, T ;

Uhles, S ;

Dagnell, M ;

Zhivotovsky, B ;

Leibiger, I ;

Grandér, D ;

Pokrovskaja, K .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (23) :24152-24162

[38] Complex modulation of cell type-specific signaling in response to type I Interferons [J].

van Boxel-Dezaire, Anette H. H. ;

Rani, M. R. Sandhya ;

Stark, George R. .

IMMUNITY, 2006, 25 (03) :361-372

[39] Control of stress-dependent cardiac growth and gene expression by a microRNA [J].

van Rooij, Eva ;

Sutherland, Lillian B. ;

Qi, Xiaoxia ;

Richardson, James A. ;

Hill, Joseph ;

Olson, Eric N. .

SCIENCE, 2007, 316 (5824) :575-579

[40] Switching from repression to activation: MicroRNAs can up-regulate translation [J].

Vasudevan, Shobha ;

Tong, Yingchun ;

Steitz, Joan A. .

SCIENCE, 2007, 318 (5858) :1931-1934

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