Journal
CELL DISCOVERY
Volume 1, Issue -, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/celldisc.2015.5
Keywords
miR-301a; Kras; NF-kappa B; Stat3; tumor microenvironment; lung cancer; colon cancer
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Funding
- National Institutes of Health (NIH) R01 grant [CA138688]
- National Natural Science Foundation of China [81270547]
- Diabetes and Obesity Center - National Institute of General Medical Sciences (NIGMS) [P20 GM103492]
- NATIONAL CANCER INSTITUTE [R01CA138688] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P20GM103492] Funding Source: NIH RePORTER
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Lung cancer and colorectal cancer account for over one-third of all cancer deaths in the United States. MicroRNA-301a (miR-301a) is an activator of both nuclear factor-kappa B ( NF-kappa B) and Stat3, and is overexpressed in both deadly malignancies. In this work, we show that genetic ablation of miR-301a reduces Kras-driven lung tumorigenesis in mice. And miR-301a deficiency protects animals from dextran sodium sulfate-induced colon inflammation and colitis-associated colon carcinogenesis. We also demonstrate that miR-301a deletion in bone marrow-derived cells attenuates tumor growth in the colon carcinogenesis model. Our findings ascertain that one microRNA-miR-301a-activates two major inflammatory pathways (NF-kappa B and Stat3) in vivo, generating a pro-inflammatory microenvironment that facilitates tumorigenesis.
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