Journal
ONCOGENE
Volume 34, Issue 6, Pages 691-703Publisher
SPRINGERNATURE
DOI: 10.1038/onc.2013.597
Keywords
miR-506; NF-kappa B p65; ROS; p53; lung cancer; selective killing
Funding
- Introduced Innovative R&D Team Program of Guangdong Province [201001Y0104789252]
- 863 Program of China [2012AA022501]
- Strategic Emerging Industry Key Technology Project of Guangdong Province [2012A080800006]
- National Natural Science Foundation of China [30870535, 90913017]
- Hundred Talents Plan of Guangzhou Municipality
- Combination Project of Guangdong Province
- Hundred Talents Plan of Guangzhou Municipality and Combination Project of Guangdong Province and the Ministry of Education [2011B090400478]
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The tumor suppressor p53, nuclear factor-kappa B (NF-kappa B) and reactive oxygen species (ROS) have crucial roles in tumorigenesis, although the mechanisms of cross talk between these factors remain largely unknown. Here we report that miR-506 upregulation occurs in 83% of lung cancer patients (156 cases), and its expression highly correlates with ROS. Ectopic expression of miR-506 inhibits NF-kappa B p65 expression, induces ROS accumulation and then activates p53 to suppress lung cancer cell viability, but not in normal cells. Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-kappa B p65 and ROS. Furthermore, we demonstrated that miR-506 mimics inhibited tumorigenesis in vivo, implicating that miR-506 might be a potential therapeutic molecule for selective killing of lung cancer cells.
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