4.3 Article

ADNCR modulates neural stem cell differentiation and proliferation through the regulation of TCF3 expression

Journal

ANNALS OF TRANSLATIONAL MEDICINE
Volume 8, Issue 15, Pages -

Publisher

AME PUBL CO
DOI: 10.21037/atm-20-1068

Keywords

Adipocyte differentiation-associated long noncoding RNA (ADNCR); long noncoding RNAs (lncRNAs); transcription factor 3 (TCF3); miR-204-5p

Funding

  1. Natural Science Foundation of China [81501117]
  2. Natural Science Foundation of Guangdong Province [2015A030310074, 2018A0303130307]
  3. Guangdong Basic and Applied Basic Research Foundation [2019A1515011739]
  4. R & D Projects in Key Areas of Guangdong Province [2018B030332001]

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Background: Neural stem cells (NSCs) are undifferentiated precursor cells that have the ability to self-renew and proliferate and have the capacity to become either glia (oligodendrocytes and astrocytes) or neurons. NSCs can act as beneficial adjuncts for many neurological disorders, such as cerebral infarction, spinal cord injuries, Alzheimer's disease, and Parkinson's disease. Long noncoding RNAs (lncRNAs) play essential roles during cell differentiation, proliferation, and metabolism. This study aimed to explore the role played by adipocyte differentiation-associated long noncoding RNA (ADNCR) in the self-renewal and multipotency of NSCs. Methods: In this study, we identified NSCs and verified that these cells were able to regenerate and differentiate into both astrocytes and neurons. Then we studied the relation between expression of ADNCR and transcription factor 3 (TCF3) and proliferation of NSCs. Results: ADNCR and TCF3 expression have been shown to decrease during the differentiation of NSCs into both neurons and astrocyte induction cells. However, the expression of the microRNA miR-204-5p increased over time during the differentiation of NSCs into both neurons and astrocyte induction cells. ADNCR acts as a competing endogenous RNA (ceRNA) for miR-204-5p, and the overexpression of ADNCR suppressed miR-204-5p expression and enhanced TCF3 expression in NSCs, which resulted in enhanced proliferation and suppressed neural differentiation. Conclusions: These data suggested that the use of ADNCR may represent a new strategy for expanding the interventions used to treat neurological disorders.

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