論文

査読有り 国際誌
2019年5月

DLL3 regulates the migration and invasion of small cell lung cancer by modulating Snail.

Cancer science
  • Megumi Furuta
  • ,
  • Hajime Kikuchi
  • ,
  • Tetsuaki Shoji
  • ,
  • Yuta Takashima
  • ,
  • Eiki Kikuchi
  • ,
  • Junko Kikuchi
  • ,
  • Ichiro Kinoshita
  • ,
  • Hirotoshi Dosaka-Akita
  • ,
  • Jun Sakakibara-Konishi

110
5
開始ページ
1599
終了ページ
1608
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/cas.13997

Delta-like protein 3 (DLL3) is a ligand of Notch signaling, which mediates cell-fate decisions and is tumor-suppressive or oncogenic depending on the cellular context. Previous studies show that DLL3 is highly expressed in small cell lung cancer (SCLC) but not in normal lung tissue, suggesting that DLL3 might be associated with neuroendocrine tumorigenesis. However, its role in SCLC remains unclear. To investigate the role of DLL3 in tumorigenesis in SCLC, we performed loss-of-function and gain-of-function assays using SCLC cell lines. In vitro analysis of cell migration and invasion by transwell assay showed that DLL3 knockdown reduced migration and invasion of SCLC cells, whereas DLL3 overexpression increased these activities. In addition, DLL3 positively regulated SNAI1 expression and knockdown of SNAI1 attenuated the migration and invasion ability of SCLC cells. Moreover, upregulated DLL3 expression induced subcutaneous tumor growth in mouse models. These results indicate that DLL3 promoted tumor growth, migration and invasion in an SCLC model by modulating SNAI1/Snail.

リンク情報
DOI
https://doi.org/10.1111/cas.13997
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/30874360
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6501010

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