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Unique haploinsufficient role of the microRNA-processing molecule Dicer1 in a murine colitis-associated tumorigenesis model

Academic Article
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Overview

authors

  • Yoshikawa, T.
  • Otsuka, M.
  • Kishikawa, T.
  • Takata, A.
  • Ohno, M.
  • Shibata, C.
  • Kang, Young Jun
  • Yoshida, H.
  • Koike, K.

publication date

  • September 2013

journal

  • PLoS One  Journal

abstract

  • 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.

subject areas

  • Animals
  • Carcinogenesis
  • Colitis
  • DEAD-box RNA Helicases
  • Disease Models, Animal
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs
  • Ribonuclease III
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Identity

PubMed Central ID

  • PMC3759383

International Standard Serial Number (ISSN)

  • 1932-6203

Digital Object Identifier (DOI)

  • 10.1371/journal.pone.0071969

PubMed ID

  • 24023722
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Additional Document Info

start page

  • e71969

volume

  • 8

issue

  • 9

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