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Modulation of tumorigenesis by the pro-inflammatory microRNA miR-301a in mouse models of lung cancer and colorectal cancer.

ABSTRACT: 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-?B (NF-?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-?B and Stat3) in vivo, generating a pro-inflammatory microenvironment that facilitates tumorigenesis.

SUBMITTER: Ma X 

PROVIDER: S-EPMC4860842 | biostudies-other | 2015

REPOSITORIES: biostudies-other

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Modulation of tumorigenesis by the pro-inflammatory microRNA miR-301a in mouse models of lung cancer and colorectal cancer.

Ma Xiaodong X   Yan Fang F   Deng Qipan Q   Li Fenge F   Lu Zhongxin Z   Liu Mofang M   Wang Lisheng L   Conklin Daniel J DJ   McCracken James J   Srivastava Sanjay S   Bhatnagar Aruni A   Li Yong Y  

Cell discovery 20150519

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-κB (NF-κB) 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 demonst  ...[more]