Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production
Summary: 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...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2021-09-01
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| Series: | iScience |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2589004221009901 |
| _version_ | 1818643001434439680 |
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| author | Koichiro Kawaguchi Kaori Komoda Ryuta Mikawa Azusa Asai Masataka Sugimoto |
| author_facet | Koichiro Kawaguchi Kaori Komoda Ryuta Mikawa Azusa Asai Masataka Sugimoto |
| author_sort | Koichiro Kawaguchi |
| collection | DOAJ |
| description | Summary: 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. |
| first_indexed | 2024-12-16T23:52:01Z |
| format | Article |
| id | doaj.art-15ef13b64d4341609c338e09b130a3af |
| institution | Directory Open Access Journal |
| issn | 2589-0042 |
| language | English |
| last_indexed | 2024-12-16T23:52:01Z |
| publishDate | 2021-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | iScience |
| spelling | doaj.art-15ef13b64d4341609c338e09b130a3af2022-12-21T22:11:18ZengElsevieriScience2589-00422021-09-01249103022Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin productionKoichiro Kawaguchi0Kaori Komoda1Ryuta Mikawa2Azusa Asai3Masataka Sugimoto4Research Institute, National Center for Geriatrics and Gerontology, Aichi 474-8511, JapanResearch Institute, National Center for Geriatrics and Gerontology, Aichi 474-8511, JapanResearch Institute, National Center for Geriatrics and Gerontology, Aichi 474-8511, JapanResearch Institute, National Center for Geriatrics and Gerontology, Aichi 474-8511, JapanResearch Institute, National Center for Geriatrics and Gerontology, Aichi 474-8511, Japan; Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan; Corresponding authorSummary: 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.http://www.sciencedirect.com/science/article/pii/S2589004221009901cell biologycancer |
| spellingShingle | Koichiro Kawaguchi Kaori Komoda Ryuta Mikawa Azusa Asai Masataka Sugimoto Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production iScience cell biology cancer |
| title | Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production |
| title_full | Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production |
| title_fullStr | Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production |
| title_full_unstemmed | Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production |
| title_short | Cellular senescence promotes cancer metastasis by enhancing soluble E-cadherin production |
| title_sort | cellular senescence promotes cancer metastasis by enhancing soluble e cadherin production |
| topic | cell biology cancer |
| url | http://www.sciencedirect.com/science/article/pii/S2589004221009901 |
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