4.7 Article

The enhancer activity of long interspersed nuclear element derived microRNA 625 induced by NF-kappa B

Journal

SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41598-021-82735-x

Keywords

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Funding

  1. Cooperative Research Program of Primate Research Institute, Kyoto University [2019-B-7]
  2. National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2018K2A9A2A08000108]
  3. JSPS
  4. NRF under the Japan-Korea Basic Scientific Cooperation Program

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Transposable elements (TEs) are DNA sequences that make up a significant portion of the human genome and generate microRNAs (miRNAs), some of which are associated with cancer. The well-known hsa-miRNA-625 is derived from long interspersed nuclear elements (LINEs), and its expression varies among different species. Analysis of the 3' UTR of GATAD2B revealed the impact of different numbers and locations of canonical binding sites on gene expression, while NF-kappa B was found to induce enhancer activity of hsa-miRNA-625-5p by sharing binding sites.
Transposable elements (TEs) are DNA sequences that cut or introduced into the genome, and they represent a massive portion of the human genome. TEs generate a considerable number of microRNAs (miRNAs) are derived from TEs (MDTEs). Numerous miRNAs are related to cancer, and hsa-miRNA-625 is a well-known oncomiR derived from long interspersed nuclear elements (LINEs). The relative expression of hsa-miRNA-625-5p differs in humans, chimpanzees, crab-eating monkeys, and mice, and four primers were designed against the 3 ' UTR of GATAD2B to analyze the different quantities of canonical binding sites and the location of miRNA binding sites. Luciferase assay was performed to score for the interaction between hsa-miRNA-625 and the 3 ' UTR of GATAD2B, while blocking NF-kappa B. In summary, the different numbers of canonical binding sites and the locations of miRNA binding sites affect gene expression, and NF-kappa B induces the enhancer activity of hsa-miRNA-625-5p by sharing the binding sites.

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