論文

査読有り 最終著者 責任著者 国際誌
2020年6月26日

Decreased miR-200b-3p in cancer cells leads to angiogenesis in HCC by enhancing endothelial ERG expression.

Scientific reports
  • Aye Moh-Moh-Aung
  • ,
  • Masayoshi Fujisawa
  • ,
  • Sachio Ito
  • ,
  • Hiroshi Katayama
  • ,
  • Toshiaki Ohara
  • ,
  • Yoko Ota
  • ,
  • Teizo Yoshimura
  • ,
  • Akihiro Matsukawa

10
1
開始ページ
10418
終了ページ
10418
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41598-020-67425-4

Transcription factor ERG (erythroblast transformation-specific (ETS)-related gene) is essential in endothelial differentiation and angiogenesis, in which microRNA (miR)-200b-3p targeting site is expected by miRNA target prediction database. miR-200b is known decreased in hepatocellular carcinoma (HCC), however, the functional relation between ERG and miR-200b-3p, originating from pre-miR-200b, in HCC angiogenesis remains unclear. We investigated whether hepatocyte-derived miR-200b-3p governs angiogenesis in HCC by targeting endothelial ERG. Levels of miR-200b-3p in HCC tissues were significantly lower than those in adjacent non-HCC tissues. Poorly differentiated HCC cell line expressed lower level of miR-200b-3p compared to well-differentiated HCC cell lines. The numbers of ERG-positive endothelial cells were higher in HCC tissues than in adjacent non-HCC tissues. There was a negative correlation between the number of ERG-positive cells and miR-200b-3p expression in HCC tissues. Culture supernatants of HCC cell lines with miR-200b-3p-overexpression reduced cell migration, proliferation and tube forming capacity in endothelial cells relative to the control, while those with miR-200b-3p-inhibition augmented the responses. Exosomes isolated from HCC culture supernatants with miR-200b-3p overexpression suppressed endothelial ERG expression. These results suggest that exosomal miR-200b-3p from hepatocytes suppresses endothelial ERG expression, and decreased miR-200b-3p in cancer cells promotes angiogenesis in HCC tissues by enhancing endothelial ERG expression.

リンク情報
DOI
https://doi.org/10.1038/s41598-020-67425-4
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32591615
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7320004
ID情報
  • DOI : 10.1038/s41598-020-67425-4
  • PubMed ID : 32591615
  • PubMed Central 記事ID : PMC7320004

エクスポート
BibTeX RIS