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Author Notes:
To whom correspondence should be addressed. Tel: +404 778 1832; Fax: +404 778 1750; Email: ywang94@emory.edu
We thank Dr. Jasin for providing the HRR reporter cell line, Dr. Pandita for providing the NHEJ reporter cell line, Dr. Allalunis-Turner for providing M059J cells and Ms. Doreen Theune for editing this manuscript.
Conflict of interest statement. None declared.
Subjects:
Research Funding:
National Institutes of Health [CA186129 to Y.W. and P30CA138292 to Winship Institute]. Funding for open access charge: National Institutes of Health [CA186129 to Y.W. and P30CA138292 to Winship Institute].
DICER-dependent biogenesis of let-7 miRNAs affects human cell response to DNA damage via targeting p21/p27.
Abstract:
Recently, it was reported that knockdown of DICER reduced the ATM-dependent DNA damage response and homologous recombination repair (HRR) via decreasing DICER-generated small RNAs at the damage sites. However, we found that knockdown of DICER dramatically increased cell resistance to camptothecin that induced damage required ATM to facilitate HRR. This phenotype is due to a prolonged G1/S transition via decreasing DICER-dependent biogenesis of miRNA let-7, which increased the p21(Waf1/Cip1)/p27(Kip1) levels and resulted in decreasing the HRR efficiency. These results uncover a novel function of DICER in regulating the cell cycle through miRNA biogenesis, thus affecting cell response to DNA damage.
Copyright information:
© The Author(s) 2015.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution of derivative works, making multiple copies, distribution, public display, and publicly performance, provided the original work is properly cited. This license requires credit be given to copyright holder and/or author, copyright and license notices be kept intact.
