論文

国際誌
2021年9月24日

Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production.

iScience
  • Koichiro Kawaguchi
  • ,
  • Kaori Komoda
  • ,
  • Ryuta Mikawa
  • ,
  • Azusa Asai
  • ,
  • Masataka Sugimoto

24
9
開始ページ
103022
終了ページ
103022
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.isci.2021.103022

Cellular senescence acts as a potent tumor-suppression mechanism in mammals; however, it also promotes tumor progression in a non-cell-autonomous manner. We provided insights into the mechanism underlying senescence-dependent metastatic cancer development. The elimination of senescent cells suppressed the lung metastasis of melanoma cells. Using an antibody array screening of humoral factor(s) that depend on cellular senescence, we identified soluble E-cadherin (seCad) as a potential mediator of the senescence-induced melanoma metastasis. seCad enhanced the invasive activity of melanoma cells both in vitro and in vivo, and gene expression profiling revealed that seCad induced genes associated with poor prognosis in patients with melanoma. An analysis of sera from patients revealed that serum seCad is associated with distant metastasis. Our data suggest that senescent cells promote metastatic lung cancer through seCad, and that seCad may be a potential diagnostic marker as well as a therapeutic target for metastatic lung cancer.

リンク情報
DOI
https://doi.org/10.1016/j.isci.2021.103022
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/34522864
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8426284
ID情報
  • DOI : 10.1016/j.isci.2021.103022
  • PubMed ID : 34522864
  • PubMed Central 記事ID : PMC8426284

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