A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.

Senescence is a universal barrier to immortalisation and tumorigenesis. As such, interest in the use of senescence-induction in a therapeutic context has been gaining momentum in the past few years; however, senescence and immortalisation remain underserved areas for drug discovery owing to a lack o...

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Main Authors: Claire J Cairney, Lauren S Godwin, Alan E Bilsland, Sharon Burns, Katrina H Stevenson, Lynn McGarry, John Revie, Jon D Moore, Ceri M Wiggins, Rebecca S Collinson, Clare Mudd, Elpida Tsonou, Mahito Sadaie, Dorothy C Bennett, Masashi Narita, Christopher J Torrance, W Nicol Keith
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-08-01
Series:PLoS Genetics
Online Access:https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1006942&type=printable
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author Claire J Cairney
Lauren S Godwin
Alan E Bilsland
Sharon Burns
Katrina H Stevenson
Lynn McGarry
John Revie
Jon D Moore
Ceri M Wiggins
Rebecca S Collinson
Clare Mudd
Elpida Tsonou
Mahito Sadaie
Dorothy C Bennett
Masashi Narita
Christopher J Torrance
W Nicol Keith
author_facet Claire J Cairney
Lauren S Godwin
Alan E Bilsland
Sharon Burns
Katrina H Stevenson
Lynn McGarry
John Revie
Jon D Moore
Ceri M Wiggins
Rebecca S Collinson
Clare Mudd
Elpida Tsonou
Mahito Sadaie
Dorothy C Bennett
Masashi Narita
Christopher J Torrance
W Nicol Keith
author_sort Claire J Cairney
collection DOAJ
description Senescence is a universal barrier to immortalisation and tumorigenesis. As such, interest in the use of senescence-induction in a therapeutic context has been gaining momentum in the past few years; however, senescence and immortalisation remain underserved areas for drug discovery owing to a lack of robust senescence inducing agents and an incomplete understanding of the signalling events underlying this complex process. In order to address this issue we undertook a large-scale morphological siRNA screen for inducers of senescence phenotypes in the human melanoma cell line A375P. Following rescreen and validation in a second cancer cell line, HCT116 colorectal carcinoma, a panel of 16 of the most robust hits were selected for further validation based on significance and the potential to be targeted by drug-like molecules. Using secondary assays for detection of senescence biomarkers p21, 53BP1 and senescence associated beta-galactosidase (SAβGal) in a panel of HCT116 cell lines carrying cancer-relevant mutations, we show that partial senescence phenotypes can be induced to varying degrees in a context dependent manner, even in the absence of p21 or p53 expression. However, proliferation arrest varied among genetic backgrounds with predominantly toxic effects in p21 null cells, while cells lacking PI3K mutation failed to arrest. Furthermore, we show that the oncogene ECT2 induces partial senescence phenotypes in all mutant backgrounds tested, demonstrating a dependence on activating KRASG13D for growth suppression and a complete senescence response. These results suggest a potential mechanism to target mutant KRAS signalling through ECT2 in cancers that are reliant on activating KRAS mutations and remain refractory to current treatments.
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spelling doaj-art-9c37fdc4728e4b2584673b3d2d9b5b8b2025-08-20T03:13:18ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042017-08-01138e100694210.1371/journal.pgen.1006942A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.Claire J CairneyLauren S GodwinAlan E BilslandSharon BurnsKatrina H StevensonLynn McGarryJohn RevieJon D MooreCeri M WigginsRebecca S CollinsonClare MuddElpida TsonouMahito SadaieDorothy C BennettMasashi NaritaChristopher J TorranceW Nicol KeithSenescence is a universal barrier to immortalisation and tumorigenesis. As such, interest in the use of senescence-induction in a therapeutic context has been gaining momentum in the past few years; however, senescence and immortalisation remain underserved areas for drug discovery owing to a lack of robust senescence inducing agents and an incomplete understanding of the signalling events underlying this complex process. In order to address this issue we undertook a large-scale morphological siRNA screen for inducers of senescence phenotypes in the human melanoma cell line A375P. Following rescreen and validation in a second cancer cell line, HCT116 colorectal carcinoma, a panel of 16 of the most robust hits were selected for further validation based on significance and the potential to be targeted by drug-like molecules. Using secondary assays for detection of senescence biomarkers p21, 53BP1 and senescence associated beta-galactosidase (SAβGal) in a panel of HCT116 cell lines carrying cancer-relevant mutations, we show that partial senescence phenotypes can be induced to varying degrees in a context dependent manner, even in the absence of p21 or p53 expression. However, proliferation arrest varied among genetic backgrounds with predominantly toxic effects in p21 null cells, while cells lacking PI3K mutation failed to arrest. Furthermore, we show that the oncogene ECT2 induces partial senescence phenotypes in all mutant backgrounds tested, demonstrating a dependence on activating KRASG13D for growth suppression and a complete senescence response. These results suggest a potential mechanism to target mutant KRAS signalling through ECT2 in cancers that are reliant on activating KRAS mutations and remain refractory to current treatments.https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1006942&type=printable
spellingShingle Claire J Cairney
Lauren S Godwin
Alan E Bilsland
Sharon Burns
Katrina H Stevenson
Lynn McGarry
John Revie
Jon D Moore
Ceri M Wiggins
Rebecca S Collinson
Clare Mudd
Elpida Tsonou
Mahito Sadaie
Dorothy C Bennett
Masashi Narita
Christopher J Torrance
W Nicol Keith
A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.
PLoS Genetics
title A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.
title_full A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.
title_fullStr A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.
title_full_unstemmed A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.
title_short A 'synthetic-sickness' screen for senescence re-engagement targets in mutant cancer backgrounds.
title_sort synthetic sickness screen for senescence re engagement targets in mutant cancer backgrounds
url https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1006942&type=printable
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