NDLI: Single-Strand Annealing in Cancer

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Single-Strand Annealing in Cancer

Content Provider	MDPI
Author	Blasiak, Janusz
Copyright Year	2021
Description	DNA double-strand breaks (DSBs) are among the most serious forms of DNA damage. In humans, DSBs are repaired mainly by non-homologous end joining (NHEJ) and homologous recombination repair (HRR). Single-strand annealing (SSA), another DSB repair system, uses homologous repeats flanking a DSB to join DNA ends and is error-prone, as it removes DNA fragments between repeats along with one repeat. Many DNA deletions observed in cancer cells display homology at breakpoint junctions, suggesting the involvement of SSA. When multiple DSBs occur in different chromosomes, SSA may result in chromosomal translocations, essential in the pathogenesis of many cancers. Inhibition of RAD52 (RAD52 Homolog, DNA Repair Protein), the master regulator of SSA, results in decreased proliferation of BRCA1/2 (BRCA1/2 DNA Repair Associated)-deficient cells, occurring in many hereditary breast and ovarian cancer cases. Therefore, RAD52 may be targeted in synthetic lethality in cancer. SSA may modulate the response to platinum-based anticancer drugs and radiation. SSA may increase the efficacy of the CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats)/Cas9 (CRISPR associated 9) genome editing and reduce its off-target effect. Several basic problems associated with SSA, including its evolutionary role, interplay with HRR and NHEJ and should be addressed to better understand its role in cancer pathogenesis and therapy.
Starting Page	2167
e-ISSN	14220067
DOI	10.3390/ijms22042167
Journal	International Journal of Molecular Sciences
Issue Number	4
Volume Number	22
Language	English
Publisher	MDPI
Publisher Date	2021-02-22
Access Restriction	Open
Subject Keyword	International Journal of Molecular Sciences Oncology Single-strand Annealing Dna Double-strand Break Repair Ssa Homologous Recombination Cancer Rad52 Synthetic Lethality Brcaness Therapeutic Genome Editing Crispr/cas9
Content Type	Text
Resource Type	Article

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