Oncogene-like addiction to aneuploidy in human cancers
Most cancers exhibit aneuploidy, but its functional significance in tumor development is controversial. Here, we describe ReDACT (Restoring Disomy in Aneuploid cells using CRISPR Targeting), a set of chromosome engineering tools that allow us to eliminate specific aneuploidies from cancer genomes. U...
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| Published in | bioRxiv |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article Paper |
| Language | English |
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Cold Spring Harbor Laboratory Press
10.01.2023
Cold Spring Harbor Laboratory |
| Edition | 1.1 |
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| Abstract | Most cancers exhibit aneuploidy, but its functional significance in tumor development is controversial. Here, we describe ReDACT (Restoring Disomy in Aneuploid cells using CRISPR Targeting), a set of chromosome engineering tools that allow us to eliminate specific aneuploidies from cancer genomes. Using ReDACT, we created a panel of isogenic cells that have or lack common aneuploidies, and we demonstrate that trisomy of chromosome 1q is required for malignant growth in cancers harboring this alteration. Mechanistically, gaining chromosome 1q increases the expression of MDM4 and suppresses TP53 signaling, and we show that TP53 mutations are mutually-exclusive with 1q aneuploidy in human cancers. Thus, specific aneuploidies play essential roles in tumorigenesis, raising the possibility that targeting these "aneuploidy addictions" could represent a novel approach for cancer treatment. |
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| AbstractList | Most cancers exhibit aneuploidy, but its functional significance in tumor development is controversial. Here, we describe ReDACT (Restoring Disomy in Aneuploid cells using CRISPR Targeting), a set of chromosome engineering tools that allow us to eliminate specific aneuploidies from cancer genomes. Using ReDACT, we created a panel of isogenic cells that have or lack common aneuploidies, and we demonstrate that trisomy of chromosome 1q is required for malignant growth in cancers harboring this alteration. Mechanistically, gaining chromosome 1q increases the expression of MDM4 and suppresses TP53 signaling, and we show that TP53 mutations are mutually-exclusive with 1q aneuploidy in human cancers. Thus, specific aneuploidies play essential roles in tumorigenesis, raising the possibility that targeting these "aneuploidy addictions" could represent a novel approach for cancer treatment.Most cancers exhibit aneuploidy, but its functional significance in tumor development is controversial. Here, we describe ReDACT (Restoring Disomy in Aneuploid cells using CRISPR Targeting), a set of chromosome engineering tools that allow us to eliminate specific aneuploidies from cancer genomes. Using ReDACT, we created a panel of isogenic cells that have or lack common aneuploidies, and we demonstrate that trisomy of chromosome 1q is required for malignant growth in cancers harboring this alteration. Mechanistically, gaining chromosome 1q increases the expression of MDM4 and suppresses TP53 signaling, and we show that TP53 mutations are mutually-exclusive with 1q aneuploidy in human cancers. Thus, specific aneuploidies play essential roles in tumorigenesis, raising the possibility that targeting these "aneuploidy addictions" could represent a novel approach for cancer treatment. Most cancers exhibit aneuploidy, but its functional significance in tumor development is controversial. Here, we describe ReDACT (Restoring Disomy in Aneuploid cells using CRISPR Targeting), a set of chromosome engineering tools that allow us to eliminate specific aneuploidies from cancer genomes. Using ReDACT, we created a panel of isogenic cells that have or lack common aneuploidies, and we demonstrate that trisomy of chromosome 1q is required for malignant growth in cancers harboring this alteration. Mechanistically, gaining chromosome 1q increases the expression of MDM4 and suppresses TP53 signaling, and we show that TP53 mutations are mutually-exclusive with 1q aneuploidy in human cancers. Thus, specific aneuploidies play essential roles in tumorigenesis, raising the possibility that targeting these "aneuploidy addictions" could represent a novel approach for cancer treatment.Competing Interest StatementJ.C.S. is a co-founder of Meliora Therapeutics, a member of the advisory board of Surface Ventures, and an employee of Google, Inc. This work was performed outside of her affiliation with Google and used no proprietary knowledge or materials from Google. J.M.S. has received consulting fees from Merck, Pfizer, Ono Pharmaceuticals, and Highside Capital Management, is a member of the advisory board of Tyra Biosciences and the Chemical Probes Portal, and is a co-founder of Meliora Therapeutics. Most cancers exhibit aneuploidy, but its functional significance in tumor development is controversial. Here, we describe ReDACT (Restoring Disomy in Aneuploid cells using CRISPR Targeting), a set of chromosome engineering tools that allow us to eliminate specific aneuploidies from cancer genomes. Using ReDACT, we created a panel of isogenic cells that have or lack common aneuploidies, and we demonstrate that trisomy of chromosome 1q is required for malignant growth in cancers harboring this alteration. Mechanistically, gaining chromosome 1q increases the expression of MDM4 and suppresses TP53 signaling, and we show that TP53 mutations are mutually-exclusive with 1q aneuploidy in human cancers. Thus, specific aneuploidies play essential roles in tumorigenesis, raising the possibility that targeting these "aneuploidy addictions" could represent a novel approach for cancer treatment. |
| Author | Hagenson, Ryan A Smith, Joan C Scaduto, Christine M Li, Wenxue Taylor, Alison M Kandikuppa, Pranav K Sausville, Erin L Lukow, Devon A Brown, Leanne M Girish, Vishruth Sheltzer, Jason M Stevens, Eric C Lee, Sophia N Salovska, Barbora Sun, Ruping Liu, Yansheng Martienssen, Robert A Mendelson, Brianna E Yuan, Monet Lou Thompson, Sarah L Lakhani, Asad A |
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| Cites_doi | 10.1101/078261 10.1007/978-3-319-20291-4_2 10.1101/2022.06.14.495959 10.1007/0-387-29362-0_23 10.1101/gr.276378.121 |
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| Notes | SourceType-Working Papers-1 ObjectType-Working Paper/Pre-Print-1 content type line 50 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 Competing Interest Statement: J.C.S. is a co-founder of Meliora Therapeutics, a member of the advisory board of Surface Ventures, and an employee of Google, Inc. This work was performed outside of her affiliation with Google and used no proprietary knowledge or materials from Google. J.M.S. has received consulting fees from Merck, Pfizer, Ono Pharmaceuticals, and Highside Capital Management, is a member of the advisory board of Tyra Biosciences and the Chemical Probes Portal, and is a co-founder of Meliora Therapeutics. |
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| Snippet | Most cancers exhibit aneuploidy, but its functional significance in tumor development is controversial. Here, we describe ReDACT (Restoring Disomy in Aneuploid... |
| SourceID | biorxiv proquest pubmed |
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| SubjectTerms | Addictions Aneuploidy Cancer Cancer Biology Chromosome 1 Chromosomes CRISPR DNA probes Genomes Oncogenes Trisomy Tumorigenesis |
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| Title | Oncogene-like addiction to aneuploidy in human cancers |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/36711674 https://www.proquest.com/docview/2763157858 https://www.proquest.com/docview/2771087277 https://www.biorxiv.org/content/10.1101/2023.01.09.523344 |
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