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...

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Main Authors: Koichiro Kawaguchi, Kaori Komoda, Ryuta Mikawa, Azusa Asai, Masataka Sugimoto
Format: Article
Language:English
Published: Elsevier 2021-09-01
Series:iScience
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2589004221009901
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spelling doaj-15ef13b64d4341609c338e09b130a3af2021-09-25T05:10:15ZengElsevieriScience2589-00422021-09-01249103022Cellular 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
collection DOAJ
language English
format Article
sources DOAJ
author Koichiro Kawaguchi
Kaori Komoda
Ryuta Mikawa
Azusa Asai
Masataka Sugimoto
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
author_facet Koichiro Kawaguchi
Kaori Komoda
Ryuta Mikawa
Azusa Asai
Masataka Sugimoto
author_sort Koichiro Kawaguchi
title 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_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_sort cellular senescence promotes cancer metastasis by enhancing soluble e-cadherin production
publisher Elsevier
series iScience
issn 2589-0042
publishDate 2021-09-01
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.
topic cell biology
cancer
url http://www.sciencedirect.com/science/article/pii/S2589004221009901
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AT azusaasai cellularsenescencepromotescancermetastasisbyenhancingsolubleecadherinproduction
AT masatakasugimoto cellularsenescencepromotescancermetastasisbyenhancingsolubleecadherinproduction
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