期刊
MOLECULAR THERAPY-NUCLEIC ACIDS
卷 24, 期 -, 页码 264-273出版社
CELL PRESS
DOI: 10.1016/j.omtn.2021.02.029
关键词
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资金
- National Natural Science Foundation of China [81970561]
- Ministry of Science and Technology of the People's Republic of China [2018ZX09201018005]
- US National Cancer Institute [2R01CA139158]
miR-26a suppresses intestinal inflammatory response by reducing NF-kB/STAT3 activation and IL-6 production, and potentially serves as a novel therapeutic target for CAC. NF-kB regulators including TLR3, PTEN, and PKCd are identified as potential targets of miR-26a.
Patients with inflammatory bowel disease are at increased risk for colitis-associated colorectal cancer (CAC). Therefore, controlling intestinal inflammation is a key therapeutic strategy for CAC. MicroRNAs (miRNAs or miRs) are a family of small noncoding RNAs that have the capacity to regulate fundamental biological processes. To date, a number of miRNAs have been identified as critical regulators of inflammation. However, the specific role of miR-26a in colonic inflammation and colitis-associated carcinogenesis is still elusive. Here, we generated mice with miR-26a myeloid-cell-specific overexpression to show that miR-26a suppressed the intestinal inflammatory response in macrophages by decreasing nuclear factor kB (NF-kB)/STAT3 activation and interleukin 6 (IL-6) production. At the molecular level, a number of NF-kB regulators, including TLR3, PTEN, and PKCd, were identified as potential targets of miR-26a. Our results thus identify a novel miRNAmediated mechanism that suppresses carcinogenic inflammation in the colon.
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