Selective targeting of KRAS oncogenic alleles by CRISPR/Cas9 inhibits proliferation of cancer cells
Open accessAbstract
Mutations within the KRAS oncogene are associated with the proliferation of various cancers. Therapeutic approaches for treating cancers with such mutations have focused on targeting the downstream protein effectors of KRAS. However, to date, no approved treatment has targeted the mutated KRAS oncogene directly. Presently, we used the selectivity of the CRISPR/Cas9 system to directly target mutated KRAS alleles. We designed single-guide RNAs (sgRNAs) to target two specific single-nucleotide missense mutations on KRAS codon-12 located in the seed region adjacent to a protospacer adjacent motif (PAM). Lentiviral transduction of Cas9 and the sgRNAs into cancer cells with respective KRAS mutations resulted in high frequency of indels in the seed region. Indel-associated disruption of the mutant KRAS alleles correlated with reduced viability of the cancer cells. The results indicate that CRISPR-Cas9-mediated genome editing can potentially be used for the treatment of cancer patients, specifically those with oncogenic KRAS mutations.
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Bang and Lee's group designed single-guide RNAs to selectively target a single-nucleotide substitution by CRISPR/Cas9 on codon-12 of KRAS in colorectal cancer cell lines.
“In 2017, Bang and Lee’s group successfully designed single-guide RNAs, compound (245), to selectively target a single-nucleotide substitution by CRISPR/Cas9 on codon-12 of KRAS in CRC cell lines.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [579]
Disrupting oncogenic KRAS alleles inhibited cancer cell growth, indicating that KRAS mutant-specific CRISPR/Cas9-mediated genome editing could potentially be adopted for cancer therapy.
“By disrupting the oncogenic alleles, cancer cell growth was inhibited, indicating that KRAS mutant-specific CRISPR/Cas9-mediated genome editing could potentially be adopted for cancer therapy.579”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [579]
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- Authors
- Lee, W., Lee, J. H., Jun, S., Lee, J. H., & Bang, D.
- Affiliations
- Yonsei University (KR)
- Corresponding author
- Lee, Ji Hyun
- Bang, Duhee
- Venue
- Scientific Reports
- Published
- 2018-08-08
- Volume
- 8
- Issue
- 1
- Pages
- 11879-11879
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6082849
- OpenAlex
- W2887986747
- Cited by
- 53
- References
- 30
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 7 · 2023: 7 · 2022: 7 · 2021: 9 · 2020: 5 · 2019: 5
- FWCI
- 1.69
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Research Foundation of Korea (NRF-2015R1A2A1A10055972, NRF-2018M3A9H3024850, NRF-2016M3A9B6948494, NRF-2015R1A2A2A03006577)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › CRISPR and Genetic Engineering
- Health Sciences › Medicine › Oncology › CAR-T cell therapy research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA regulation and disease
- Keywords
- KRAS mutation, CRISPR/Cas9 genome editing, single guide RNA design, protospacer adjacent motif, indels, lentiviral gene delivery, tumor cell proliferation
- MeSH terms
- Gene Editing, RNA, Guide, CRISPR-Cas Systems, Alleles, Cell Line, Codon, Humans, Mutation, Proto-Oncogene Proteins p21(ras), Cell Line, Tumor, Cell Proliferation, HEK293 Cells, Clustered Regularly Interspaced Short Palindromic Repeats, CRISPR-Cas Systems
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