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dc.contributor.author
Guccini, Ilaria
dc.contributor.author
Borrelli, Costanza
dc.contributor.author
Moor, Andreas E.
dc.contributor.author
Alimonti, Andrea
dc.contributor.author
et al.
dc.date.accessioned
2021-01-26T12:33:25Z
dc.date.available
2021-01-10T03:40:51Z
dc.date.available
2021-01-13T08:59:46Z
dc.date.available
2021-01-26T12:33:25Z
dc.date.issued
2021-01-11
dc.identifier.issn
1535-6108
dc.identifier.issn
1878-3686
dc.identifier.other
10.1016/j.ccell.2020.10.012
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/460880
dc.description.abstract
Metastases account for most cancer-related deaths, yet the mechanisms underlying metastatic spread remain poorly understood. Recent evidence demonstrates that senescent cells, while initially restricting tumorigenesis, can induce tumor progression. Here, we identify the metalloproteinase inhibitor TIMP1 as a molecular switch that determines the effects of senescence in prostate cancer. Senescence driven either by PTEN deficiency or chemotherapy limits the progression of prostate cancer in mice. TIMP1 deletion allows senescence to promote metastasis, and elimination of senescent cells with a senolytic BCL-2 inhibitor impairs metastasis. Mechanistically, TIMP1 loss reprograms the senescence-associated secretory phenotype (SASP) of senescent tumor cells through activation of matrix metalloproteinases (MMPs). Loss of PTEN and TIMP1 in prostate cancer is frequent and correlates with resistance to docetaxel and worst clinical outcomes in patients treated in an adjuvant setting. Altogether, these findings provide insights into the dual roles of tumor-associated senescence and can potentially impact the treatment of prostate cancer. © 2020 Elsevier
en_US
dc.language.iso
en
en_US
dc.publisher
Cell Press
en_US
dc.title
Senescence Reprogramming by TIMP1 Deficiency Promotes Prostate Cancer Metastasis
en_US
dc.type
Journal Article
dc.date.published
2020-11-12
ethz.journal.title
Cancer Cell
ethz.journal.volume
39
en_US
ethz.journal.issue
1
en_US
ethz.journal.abbreviated
Cancer cell (Print)
ethz.pages.start
68
en_US
ethz.pages.end
82.e9
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
Cambridge, MA
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02060 - Dep. Biosysteme / Dep. of Biosystems Science and Eng.::09711 - Moor, Andreas / Moor, Andreas
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03739 - Stoffel, Markus / Stoffel, Markus
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03739 - Stoffel, Markus / Stoffel, Markus
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03630 - Krek, Wilhelm (ehemalig) / Krek, Wilhelm (former)
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02060 - Dep. Biosysteme / Dep. of Biosystems Science and Eng.::09711 - Moor, Andreas / Moor, Andreas
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03630 - Krek, Wilhelm (ehemalig) / Krek, Wilhelm (former)
ethz.date.deposited
2021-01-10T03:40:55Z
ethz.source
SCOPUS
ethz.eth
yes
en_US
ethz.availability
Metadata only
en_US
ethz.rosetta.installDate
2021-01-13T08:59:57Z
ethz.rosetta.lastUpdated
2022-03-29T04:58:33Z
ethz.rosetta.versionExported
true
ethz.COinS
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