Cited by 31MicroRNA in disease regulationNeurogenesis and neuroplasticity mechanismsDevelopmental Biology and Gene Regulation

Functional analysis of microRNAs during the retinoic acid-induced neuronal differentiation of human NT2 cells

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Kawasaki, H., Taira, K.·2003·Nucleic Acids Symposium Series

Abstract

MicroRNAs (miRNAs) are phylogenetically widespread small RNAs in animals and plants. These small RNAs can regulate a gene expression at a translational level and play roles during the development of C. elegans, D. melanogaster and plants. Although more than two hundred miRNAs have been found in mammals, the target mRNAs of miRNAs is unknown. Recently, we identified Hes1, bHLH transcriptional repressor, as a target of miR-23 in NT2 cells. In this study, we further investigate that the expression of Hes1 is regulated by miR-23 during the retinoic acid (RA)-induced neural differentiation of NT2 cells. Reduction in the level of miR-23 by siRNAs resulted in the accumulation of Hes1 in differentiated NT2 cells. Moreover, a reduction in the level of miR-23 by siRNA-miR-23 affected the RA-induced neural differentiation of NT2 cells. Thus, our results indicate that miR-23 has a critical role in the RA-induced neuronal differentiation of NT2 cells.

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Crossref · 10.1093/nass/3.1.243

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  • Regulation of neural development by miR-23 is probably achieved through the combined action of other miRNAs.

    “It indicates that the regulation of neural development by miR-23 is probably achieved through the combined action of other miRNAs.”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [130]

    The Results and Discussion (page not supplied) say that miR-23 plays a critical role in retinoic-acid-induced neuronal differentiation of NT2 cells. The paper does not say that this role is achieved through combined action with other miRNAs; searches for combined action and cooperation found no such passage. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Expression level of Hes1 increases, ultimately hindering neuronal differentiation of P19 cells induced by retinoic acid.

    “The expression level of Hes1 increases, ultimately hindering neuronal differentiation of P19 cells induced by the retinoic acid [[129], [130], [131]].”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [130]

    The Results and Discussion (page not specified in the supplied copy) report increased Hes1 protein and failure of retinoic-acid-induced neural differentiation after miR-23 was reduced. Those experiments used human NT2 cells, not P19 cells, and the paper does not establish that increased Hes1 itself caused the failure to differentiate. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Hes1 is also directly targeted by miR-124, and knockdown of miR-124 levels mediated by locked nucleic acids is similar to the effect of miR-23 inhibition.

    “Hes1 is also directly targeted by miR-124, and the knockdown of miR-124 levels mediated by locked nucleic acids is similar to the effect of miR-23 inhibition.”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [130]

    The Results and Discussion (page unavailable in our copy) report that inhibiting miR-23 with synthetic siRNA increased Hes1 protein and impeded neuronal differentiation. The paper does not report that miR-124 directly targets Hes1, or test locked-nucleic-acid knockdown of miR-124 against the effect of miR-23 inhibition. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Decrease in miR-23 levels can lead to accumulation of Hes1 during retinal acid-induced neural differentiation in NT2 cells, which in turn affects neural differentiation.

    “The decrease in miR-23 levels can lead to the accumulation of Hes1 during retinal acid-induced neural differentiation in NT2 cells, which in turn affects neural differentiation.”
  • Hes1 is an authentic target of miR-23.

    “A basic helix-loop-helix transcriptional repressor, named Hes1, is an authentic target of miR-23.”

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Cited by 31

Research works printed but not linked: 1

  1. Kawasaki, H. and Taira, K. (2003) Nature. in press.

Authors
Kawasaki, H., & Taira, K.
Affiliations
The University of Tokyo (JP)
Venue
Nucleic Acids Symposium Series
Published
2003-09-01
Volume
3
Issue
1
Pages
243-244
ISSN
  • 0261-3166 (ISSN-L)
  • 1746-8272
OpenAlex
W2121019724
Cited by
31
References
0
Citations by year
2025: 2 · 2024: 1 · 2021: 1 · 2020: 1 · 2019: 2 · 2014: 3 · 2013: 1 · 2012: 2
FWCI
25.83
Type
conference paper
Language
en
Open access
Locations
  • Nucleic Acids Symposium Series (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Keywords
microRNA, miR-23, retinoic acid, neuronal differentiation, NT2 cells, Hes1, bHLH transcription factors, translational regulation, siRNA knockdown, neural development
MeSH terms
Cell Differentiation, Cell Line, Humans, Neurons, Tretinoin, MicroRNAs

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