期刊
PLOS ONE
卷 8, 期 9, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0071969
关键词
-
资金
- Ministry of Education, Culture, Sports, Science and Technology, Japan [22390058, 2529307, 24390183]
- Health Sciences Research Grants of The Ministry of Health, Labour and Welfare of Japan
- Japan Foundation for Applied Enzymology
- Sagawa Foundation for Promotion of Cancer Research
- Cell Science Research Foundation
- Japanese Society of Gastroenterology
- Grants-in-Aid for Scientific Research [25860520, 24390183, 25293076, 22390058] Funding Source: KAKEN
A widespread downregulated expression of microRNAs (miRNAs) is commonly observed in human cancers. Similarly, deregulated expression of miRNA-processing pathway components, which results in the reduction of global miRNA expression, may also be associated with tumorigenesis. Here, we show that specific ablation of Dicer1 in intestinal epithelial cells accelerates intestinal inflammation-associated tumorigenesis. This effect was apparent only when a single copy of Dicer1 was deleted, but not with complete Dicer1 ablation. DICER expression and subsequent mature miRNA levels were inversely correlated with the number of intact Dicer1 alleles. Because the expression levels of DICER were retained in tumors and its surrounding tissues even after induction of colitis-associated tumors, the effects of Dicer1 deletion were cell-autonomous. Although the expression levels of representative oncogenes and tumor suppressor genes were in most cases inversely correlated with the expression levels of DICER, some genes were not affected by Dicer1 deletion. Thus, deregulating the delicate balance between the expression levels of tumor-promoting and - suppressive genes may be crucial for tumorigenesis in this unique haploinsufficient case.
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