High-Throughput Functional Genetic and Compound Screens Identify Targets for Senescence Induction in Cancer

Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer cells to undergo senescence are unclear. Here, we use both functional genetic and compound screens in cancer cells harboring a reporter that...

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Vydané v:	Cell reports (Cambridge) Ročník 21; číslo 3; s. 773 - 783
Hlavní autori:	Wang, Liqin, Leite de Oliveira, Rodrigo, Wang, Cun, Fernandes Neto, João M., Mainardi, Sara, Evers, Bastiaan, Lieftink, Cor, Morris, Ben, Jochems, Fleur, Willemsen, Lisa, Beijersbergen, Roderick L., Bernards, René
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Elsevier Inc 17.10.2017 Elsevier
Predmet:	aurora kinase Aurora Kinases - antagonists & inhibitors Aurora Kinases - metabolism Cell Line, Tumor Cellular Senescence - drug effects Cellular Senescence - genetics compound screen CRISPR-Cas Systems - genetics Down-Regulation - genetics Gene Knockout Techniques Genes, Reporter genetic screens Genetic Testing Green Fluorescent Proteins - metabolism High-Throughput Screening Assays Humans Melanoma - genetics Melanoma - pathology miR146 Neoplasms - genetics Neoplasms - pathology Oncogenes Protein Kinase Inhibitors - pharmacology Receptor, Epidermal Growth Factor - metabolism senescence senolysis SMARCB1 Protein - genetics SOXE Transcription Factors - genetics SOXE Transcription Factors - metabolism SWI/SNF senescence miR146 SWI/SNF aurora kinase genetic screens compound screen senolysis
ISSN:	2211-1247, 2211-1247
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Abstract	Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer cells to undergo senescence are unclear. Here, we use both functional genetic and compound screens in cancer cells harboring a reporter that is activated during senescence to find targets that induce senescence. We show that suppression of the SWI/SNF component SMARCB1 induces senescence in melanoma through strong activation of the MAP kinase pathway. From the compound screen, we identified multiple aurora kinase inhibitors as potent inducers of senescence in RAS mutant lung cancer. Senescent melanoma and lung cancer cells acquire sensitivity to the BCL2 family inhibitor ABT263. We propose a one-two punch approach for the treatment of cancer in which a drug is first used to induce senescence in cancer cells and a second drug is then used to kill senescent cancer cells. [Display omitted] •CRISPR and chemical screens identify senescence inducers in cancer cells•SMARCB1 knockout induces senescence in melanoma•Aurora kinase inhibition induces senescence in multiple cancer types•Senescent cancer cells become vulnerable to killing by ABT263 Wang et al. find that CRISPR-mediated genetic screens and chemical screens serve as two types of high-throughput methods to identify senescence inducers in cancer cells. They also show that senescent cancer cells can be killed selectively by the BCL2-family inhibitor ABT263, providing a potential sequential drug treatment strategy for cancer.
AbstractList	Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer cells to undergo senescence are unclear. Here, we use both functional genetic and compound screens in cancer cells harboring a reporter that is activated during senescence to find targets that induce senescence. We show that suppression of the SWI/SNF component SMARCB1 induces senescence in melanoma through strong activation of the MAP kinase pathway. From the compound screen, we identified multiple aurora kinase inhibitors as potent inducers of senescence in RAS mutant lung cancer. Senescent melanoma and lung cancer cells acquire sensitivity to the BCL2 family inhibitor ABT263. We propose a one-two punch approach for the treatment of cancer in which a drug is first used to induce senescence in cancer cells and a second drug is then used to kill senescent cancer cells.Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer cells to undergo senescence are unclear. Here, we use both functional genetic and compound screens in cancer cells harboring a reporter that is activated during senescence to find targets that induce senescence. We show that suppression of the SWI/SNF component SMARCB1 induces senescence in melanoma through strong activation of the MAP kinase pathway. From the compound screen, we identified multiple aurora kinase inhibitors as potent inducers of senescence in RAS mutant lung cancer. Senescent melanoma and lung cancer cells acquire sensitivity to the BCL2 family inhibitor ABT263. We propose a one-two punch approach for the treatment of cancer in which a drug is first used to induce senescence in cancer cells and a second drug is then used to kill senescent cancer cells. Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer cells to undergo senescence are unclear. Here, we use both functional genetic and compound screens in cancer cells harboring a reporter that is activated during senescence to find targets that induce senescence. We show that suppression of the SWI/SNF component SMARCB1 induces senescence in melanoma through strong activation of the MAP kinase pathway. From the compound screen, we identified multiple aurora kinase inhibitors as potent inducers of senescence in RAS mutant lung cancer. Senescent melanoma and lung cancer cells acquire sensitivity to the BCL2 family inhibitor ABT263. We propose a one-two punch approach for the treatment of cancer in which a drug is first used to induce senescence in cancer cells and a second drug is then used to kill senescent cancer cells. [Display omitted] •CRISPR and chemical screens identify senescence inducers in cancer cells•SMARCB1 knockout induces senescence in melanoma•Aurora kinase inhibition induces senescence in multiple cancer types•Senescent cancer cells become vulnerable to killing by ABT263 Wang et al. find that CRISPR-mediated genetic screens and chemical screens serve as two types of high-throughput methods to identify senescence inducers in cancer cells. They also show that senescent cancer cells can be killed selectively by the BCL2-family inhibitor ABT263, providing a potential sequential drug treatment strategy for cancer. Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer cells to undergo senescence are unclear. Here, we use both functional genetic and compound screens in cancer cells harboring a reporter that is activated during senescence to find targets that induce senescence. We show that suppression of the SWI/SNF component SMARCB1 induces senescence in melanoma through strong activation of the MAP kinase pathway. From the compound screen, we identified multiple aurora kinase inhibitors as potent inducers of senescence in RAS mutant lung cancer. Senescent melanoma and lung cancer cells acquire sensitivity to the BCL2 family inhibitor ABT263. We propose a one-two punch approach for the treatment of cancer in which a drug is first used to induce senescence in cancer cells and a second drug is then used to kill senescent cancer cells.
Author	Jochems, Fleur Fernandes Neto, João M. Morris, Ben Beijersbergen, Roderick L. Wang, Liqin Wang, Cun Leite de Oliveira, Rodrigo Mainardi, Sara Evers, Bastiaan Willemsen, Lisa Lieftink, Cor Bernards, René
Author_xml	– sequence: 1 givenname: Liqin surname: Wang fullname: Wang, Liqin organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 2 givenname: Rodrigo surname: Leite de Oliveira fullname: Leite de Oliveira, Rodrigo organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 3 givenname: Cun surname: Wang fullname: Wang, Cun organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 4 givenname: João M. surname: Fernandes Neto fullname: Fernandes Neto, João M. organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 5 givenname: Sara surname: Mainardi fullname: Mainardi, Sara organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 6 givenname: Bastiaan surname: Evers fullname: Evers, Bastiaan organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 7 givenname: Cor surname: Lieftink fullname: Lieftink, Cor organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 8 givenname: Ben surname: Morris fullname: Morris, Ben organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 9 givenname: Fleur surname: Jochems fullname: Jochems, Fleur organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 10 givenname: Lisa surname: Willemsen fullname: Willemsen, Lisa organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 11 givenname: Roderick L. surname: Beijersbergen fullname: Beijersbergen, Roderick L. organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands – sequence: 12 givenname: René surname: Bernards fullname: Bernards, René email: r.bernards@nki.nl organization: Division of Molecular Carcinogenesis, Cancer Genomics Centre, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, the Netherlands
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Snippet	Senescence is a proliferation arrest that can result from a variety of stresses. Cancer cells can also undergo senescence, but the stresses that provoke cancer...
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SubjectTerms	aurora kinase Aurora Kinases - antagonists & inhibitors Aurora Kinases - metabolism Cell Line, Tumor Cellular Senescence - drug effects Cellular Senescence - genetics compound screen CRISPR-Cas Systems - genetics Down-Regulation - genetics Gene Knockout Techniques Genes, Reporter genetic screens Genetic Testing Green Fluorescent Proteins - metabolism High-Throughput Screening Assays Humans Melanoma - genetics Melanoma - pathology miR146 Neoplasms - genetics Neoplasms - pathology Oncogenes Protein Kinase Inhibitors - pharmacology Receptor, Epidermal Growth Factor - metabolism senescence senolysis SMARCB1 Protein - genetics SOXE Transcription Factors - genetics SOXE Transcription Factors - metabolism SWI/SNF
Title	High-Throughput Functional Genetic and Compound Screens Identify Targets for Senescence Induction in Cancer
URI	https://dx.doi.org/10.1016/j.celrep.2017.09.085 https://www.ncbi.nlm.nih.gov/pubmed/29045843 https://www.proquest.com/docview/1953297708 https://doaj.org/article/6000ab834242421891249fb41a57f78a
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