miR-9 and let-7g enhance the sensitivity to ionizing radiation by suppression of NFkappaB1.
10.3858/emm.2011.43.5.031
- Author:
Himanshu ARORA
1
;
Rehana QURESHI
;
Shunzi JIN
;
Ae Kyoung PARK
;
Woong Yang PARK
Author Information
1. Laboratory of Molecular and Genomic Medicine, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 110-799, Korea. wypark@snu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
ionizing radiation;
let-7g;
lung cancer;
miR-9;
NFkappaB1
- MeSH:
Base Sequence;
Cell Line, Tumor;
Cell Survival/genetics/radiation effects;
Gene Expression Profiling;
*Gene Expression Regulation, Neoplastic/radiation effects;
Humans;
Lung Neoplasms/genetics/metabolism;
MicroRNAs/genetics/*metabolism;
NF-kappa B p50 Subunit/genetics/*metabolism;
Radiation Tolerance/*genetics;
Radiation, Ionizing;
Sequence Alignment
- From:Experimental & Molecular Medicine
2011;43(5):298-304
- CountryRepublic of Korea
- Language:English
-
Abstract:
The activation of nuclear factor-kappa B1 (NFkappaB1) in cancer cells may confer resistance to ionizing radiation (IR). To enhance the therapeutic efficiency of IR in lung cancer, we screened for microRNAs (miRNAs) that suppress NFkappaB1 and observed their effects on radiosensitivity in a human lung cancer cell line. From time series data of miRNA expression in gamma-irradiated H1299 human lung cancer cells, we found that the expression of miR-9 was inversely correlated with that of NFkappaB1. Overexpression of miR-9 down-regulated the level of NFkappaB1 in H1299 cells, and the surviving fraction of gamma-irradiated cells was decreased. Interestingly, let-7g also suppressed the expression of NFkappaB1, although there was no canonical target site for let-7g in the NFkappaB1 3' untranslated region. From these results, we conclude that the expression of miR-9 and let-7g could enhance the efficiency of radiotherapy for lung cancer treatment through the inhibition of NFkappaB1.
