2021年9月24日
Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production.
iScience
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- 巻
- 24
- 号
- 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
- ID情報
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- DOI : 10.1016/j.isci.2021.103022
- PubMed ID : 34522864
- PubMed Central 記事ID : PMC8426284