Treating ARID1A mutated cancers by harnessing synthetic lethality and DNA damage response
Open accessAbstract
Chromatin remodeling is an essential cellular process for organizing chromatin structure into either open or close configuration at specific chromatin locations by orchestrating and modifying histone complexes. This task is responsible for fundamental cell physiology including transcription, DNA replication, methylation, and damage repair. Aberrations in this activity have emerged as epigenomic mechanisms in cancer development that increase tumor clonal fitness and adaptability amidst various selection pressures. Inactivating mutations in AT-rich interaction domain 1A (ARID1A), a gene encoding a large nuclear protein member belonging to the SWI/SNF chromatin remodeling complex, result in its loss of expression. ARID1A is the most commonly mutated chromatin remodeler gene, exhibiting the highest mutation frequency in endometrium-related uterine and ovarian carcinomas. As a tumor suppressor gene, ARID1A is essential for regulating cell cycle, facilitating DNA damage repair, and controlling expression of genes that are essential for maintaining cellular differentiation and homeostasis in non-transformed cells. Thus, ARID1A deficiency due to somatic mutations propels tumor progression and dissemination. The recent success of PARP inhibitors in treating homologous recombination DNA repair-deficient tumors has engendered keen interest in developing synthetic lethality-based therapeutic strategies for ARID1A-mutated neoplasms. In this review, we summarize recent advances in understanding the biology of ARID1A in cancer development, with special emphasis on its roles in DNA damage repair. We also discuss strategies to harness synthetic lethal mechanisms for future therapeutics against ARID1A-mutated cancers.
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ARID1A regulates DNA damage checkpoints and sensitizes cells to DNA damage response (DDR) targeting agents.
“ARID1A regulates DNA damage checkpoints and sensitizes cells to DNA damage response (DDR) targeting agents67–69.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [67]
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Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma
Yousef, A., Yousef, M., Chowdhury, S., Abdilleh, K., Knafl, M., Edelkamp, P., Alfaro-Munoz, K., Chacko, R., Peterson, J., Smaglo, B. G., et al. (2024) · npj Precision Oncology · doi:10.1038/s41698-024-00505-0 · Cited by 93 · see citing works
- Authors
- Mandal, J., Mandal, P., Wang, T.-L., & Shih, I.-M.
- Affiliations
- Johns Hopkins University (US)
- B.P. Koirala Institute of Health Sciences (NP)
- Corresponding author
- Wang, Tian-Li
- Shih, Ie-Ming
- Venue
- Journal of Biomedical Science
- Published
- 2022-09-19
- Volume
- 29
- Issue
- 1
- Pages
- 71-71
- ISSN
- 1021-7770 (ISSN-L)
- 1423-0127
- PMC
- PMC9484255
- OpenAlex
- W4296457167
- Cited by
- 84
- References
- 124
- Citations by year
- 2026: 13 · 2025: 25 · 2024: 26 · 2023: 20
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- Journal of Biomedical Science (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Johns Hopkins University
- NIH/NCI (P50CA22899, CA215483)
- Richard W. TeLinde Endowment
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- ARID1A, SWI/SNF complex, synthetic lethality, DNA damage response, PARP inhibitors, endometrial cancer, ovarian carcinoma, tumor suppressor, chromatin remodeling, DNA repair deficiency, cancer therapy
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Synthetic Lethal Mutations, Chromatin, DNA Damage, DNA-Binding Proteins, Female, Histones, Humans, Nuclear Proteins, Ovarian Neoplasms, Transcription Factors
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