VRK1 as a synthetic lethal target in VRK2 promoter-methylated cancers of the nervous system
Open accessAbstract
Collateral lethality occurs when loss of a gene/protein renders cancer cells dependent on its remaining paralog. Combining genome-scale CRISPR/Cas9 loss-of-function screens with RNA sequencing in over 900 cancer cell lines, we found that cancers of nervous system lineage, including adult and pediatric gliomas and neuroblastomas, required the nuclear kinase vaccinia-related kinase 1 (VRK1) for their survival in vivo. VRK1 dependency was inversely correlated with expression of its paralog VRK2 . VRK2 knockout sensitized cells to VRK1 loss, and conversely, VRK2 overexpression increased cell fitness in the setting of VRK1 loss. DNA methylation of the VRK2 promoter was associated with low VRK2 expression in human neuroblastomas and adult and pediatric gliomas. Mechanistically, depletion of VRK1 reduced barrier-to-autointegration factor phosphorylation during mitosis, resulting in DNA damage and apoptosis. Together, these studies identify VRK1 as a synthetic lethal target in VRK2 promoter–methylated adult and pediatric gliomas and neuroblastomas.
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RIOK2 is a relatively unexplored RSK target whose normal function is to promote maturation of the 40S ribosome.
“RIOK2 is a relatively unexplored RSK target whose normal function is to promote maturation of the 40S ribosome (69).”
From Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy (2023) · cites this paper as [69]
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- Authors
- So, J., Mabe, N. W., Englinger, B., Chow, K.-H., Moyer, S. M., Yerrum, S., Trissal, M. C., Marques, J. G., Kwon, J. J., Shim, B., Pal, S., Panditharatna, E., Quinn, T., Schaefer, D. A., Jeong, D., Mayhew, D. L., Hwang, J., Beroukhim, R., Ligon, K. L., Stegmaier, K., Filbin, M. G., & Hahn, W. C.
- Affiliations
- Broad Institute (US)
- Harvard University (US)
- University of Minnesota (US)
- Corresponding author
- Stegmaier, Kimberly
- Filbin, Mariella G.
- Hahn, William C.
- ORCID
- So, Jonathan
- Mabe, Nathaniel W.
- Englinger, Bernhard
- Moyer, Sydney M.
- Trissal, Maria C.
- Marques, Joana G.
- Kwon, Jason J.
- Shim, Brian
- Pal, Sangita
- Panditharatna, Eshini
- Schaefer, Daniel A.
- Jeong, Daeun
- Mayhew, David L.
- Hwang, Justin
- Beroukhim, Rameen
- Ligon, Keith L.
- Stegmaier, Kimberly
- Filbin, Mariella G.
- Hahn, William C.
- Venue
- JCI Insight
- Published
- 2022-10-10
- Volume
- 7
- Issue
- 19
- ISSN
- 2379-3708 (ISSN-L)
- PMC
- PMC9675470
- OpenAlex
- W4293582075
- Cited by
- 45
- References
- 52
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 22 · 2023: 11 · 2022: 1
- FWCI
- 6.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- JCI Insight (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Cancer Institute (R25 CA174650, F32 CA243290, F32 CA261035)
- Austrian Science Fund (J-4311)
- National Institutes of Health (U01 CA176058, R03 TR 003343, R35 CA210030, P01 CA217959)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- VRK1, VRK2, synthetic lethality, glioma, neuroblastoma, DNA methylation, promoter methylation, apoptosis, tumor cell survival, CRISPR-Cas9 loss-of-function screen, nervous system cancer
- MeSH terms
- Child, Glioma, Humans, Nervous System, Neuroblastoma, Vaccinia, Vaccinia virus, Protein Serine-Threonine Kinases, Intracellular Signaling Peptides and Proteins
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