A Comparative Genomic Approach for Identifying Synthetic Lethal Interactions in Human Cancer
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Abstract
Synthetic lethal interactions enable a novel approach for discovering specific genetic vulnerabilities in cancer cells that can be exploited for the development of therapeutics. Despite successes in model organisms such as yeast, discovering synthetic lethal interactions on a large scale in human cells remains a significant challenge. We describe a comparative genomic strategy for identifying cancer-relevant synthetic lethal interactions whereby candidate interactions are prioritized on the basis of genetic interaction data available in yeast, followed by targeted testing of candidate interactions in human cell lines. As a proof of principle, we describe two novel synthetic lethal interactions in human cells discovered by this approach, one between the tumor suppressor gene SMARCB1 and PSMA4, and another between alveolar soft-part sarcoma-associated ASPSCR1 and PSMC2. These results suggest therapeutic targets for cancers harboring mutations in SMARCB1 or ASPSCR1 and highlight the potential of a targeted, cross-species strategy for identifying synthetic lethal interactions relevant to human cancer. Cancer Res; 73(20); 6128–36. ©2013 AACR.
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Conservation of genetic interactions from yeast to human cells has been observed, particularly within fundamental bioprocesses like DNA synthesis and repair and chromosome segregation.
“conservation of genetic interactions from yeast to human cells has been observed (51, 52), particularly within fundamental bioprocesses like DNA synthesis and repair and chromosome segregation”
From A global genetic interaction network maps a wiring diagram of cellular function (2016) · cites this paper as [51]
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- Authors
- Deshpande, R., Asiedu, M. K., Klebig, M., Sutor, S., Kuzmin, E., Nelson, J., Piotrowski, J., Ho Shin, S., Yoshida, M., Costanzo, M., Boone, C., Wigle, D. A., & Myers, C. L.
- Affiliations
- University of Minnesota (US)
- Authors' Affiliations: 1Department of Computer Science and Engineering; 2Program in Biomedical Informatics and Computational Biology, University of Minnesota, Minneapolis; 3Department of Surgery, Mayo Clinic, Rochester, Minnesota; 4Department of Laboratory Medicine & Pathology, Molecular Genetics Lab, Mayo Clinic, Rochester, Minnesota; 5Department of Molecular Genetics, Terrence Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Ontario, Canada; 6Chemical Genomics Research Group, RIKEN Advance Science Institute, Saitama, Japan; and 7Great Lakes Bioenergy Research Center, University of Wisconsin, Madison, Wisconsin
- Corresponding author
- Wigle, Dennis A.
- ORCID
- Venue
- Cancer Research
- Published
- 2013-10-14
- Volume
- 73
- Issue
- 20
- Pages
- 6128-6136
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC3809957
- OpenAlex
- W2137906640
- Cited by
- 64
- References
- 34
- Citations by year
- 2025: 5 · 2024: 3 · 2023: 1 · 2022: 5 · 2021: 5 · 2020: 2 · 2019: 9 · 2018: 7 · 2017: 8 · 2016: 7 · 2015: 7 · 2014: 5
- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research (MOP97939, MOP-10262, MOP-57830)
- National Human Genome Research Institute (R01HG005084, R01HG005853)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- synthetic lethality, human cancer, comparative genomics, SMARCB1, PSMA4, ASPSCR1, alveolar soft part sarcoma, tumor suppressor, therapeutic target, genetic susceptibility
- MeSH terms
- SMARCB1 Protein, Animals, Chromosomal Proteins, Non-Histone, DNA-Binding Proteins, Humans, Neoplasms, Transcription Factors, Cell Culture Techniques, Genomics, RNA, Small Interfering
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