Cancer therapeutic targeting using mutant–p53-specific siRNAs
Open accessAbstract
Mutations in Tp53 compromise therapeutic response, due either to the dominant-negative effect over the functional wild-type allele; or as a result of the survival advantage conferred by mutant p53 to which cancer cells become addicted. Thus, targeting mutant p53 represents an effective therapeutic strategy to treat over half of all cancers. We have therefore generated a series of small-interfering-RNAs, capable of targeting four p53 hot-spot mutants which represent ~20% of all p53 mutations. These mutant-p53-specific siRNAs (MupSi) are highly specific in silencing the expression of the intended mutants without affecting wild-type p53. Functionally, these MupSis induce cell death by abrogating both the addiction to mutant p53 and the dominant-negative effect; and retard tumor growth in xenografts when administered in a therapeutic setting. These data together demonstrate the possibility of targeting mutant p53 specifically to improve clinical outcome.
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Some mutant p53-specific siRNAs elevate the dominant-negative activity of mutant p53 over wild-type p53, sensitize tumor cells to treatment, abrogate tumor-cell addiction to mutant p53, promote cancer cell death, and retard tumor growth in patient-derived xenografts without side effects or organ toxicity.
“Some of these mutant p53-specific siRNAs have been shown to elevate the dominant-negative activity of mutant p53 over the wild-type form, such as compound (240), thus sensitize tumor cells to therapeutic treatment, abrogating the addiction of tumor cells to mutant p53 for survival, promoting cell death of cancer cells expressing mutant p53, and retarding tumor growth in patient-derived xenografts”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [574]
Sabapathy and colleagues designed a series of siRNAs that selectively target four p53 hot-spot mutants.
“In 2019, Kanaga Sabapathy and colleagues designed a series of siRNAs that selectively target four p53 hot-spot mutants.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [574]
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- Authors
- Ubby, I., Krueger, C., Rosato, R., Qian, W., Chang, J., & Sabapathy, K.
- Affiliations
- National Cancer Centre Singapore (SG)
- Houston Methodist (US)
- National University of Singapore (SG)
- Corresponding author
- Sabapathy, Kanaga
- Venue
- Oncogene
- Published
- 2019-01-14
- Volume
- 38
- Issue
- 18
- Pages
- 3415-3427
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC6756012
- OpenAlex
- W4238398857
- Cited by
- 50
- References
- 54
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 8 · 2023: 11 · 2022: 4 · 2021: 8 · 2020: 3 · 2019: 3
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Oncogene (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- MOH | National Medical Research Council
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- mutant p53, siRNA, siRNA therapeutics, TP53 mutation, dominant negative effect, cancer therapy, tumor growth inhibition, xenografts, cell death
- MeSH terms
- Alleles, Animals, Humans, Mutation, Tumor Suppressor Protein p53, Mice, SCID, Cell Death, RNA, Small Interfering, Cell Proliferation, Mice
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