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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2023.5
- 수록면
- 265 - 274 (10page)
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Defects in DNA double-strand break (DSB) repair signaling permitcancer cells to accumulate genomic alterations that confertheir aggressive phenotype. Nevertheless, tumors depend on residualDNA repair abilities to survive the DNA damage inducedby genotoxic stress. This is why only isolated DNA repair signalingis inactivated in cancer cells. DNA DSB repair signalingcontributes to general mechanism for various types of lesionsin diverse cell cycle phases. DNA DSB repair genes are frequentlymutated and amplified in cancer; however, limited data existregarding the overall genomic prospect and functional result ofthese modifications. We list the DNA repair genes and relatedE3 ligases. Mutation and expression frequencies of these geneswere analyzed in COSMIC and TCGA. The 11 genes with a highfrequency of mutation differed between cancers, and mutationsin many DNA DSB repair E3 ligase genes were related to ahigher total mutation burden. DNA DSB repair E3 ligase genesare involved in tumor suppressive or oncogenic functions, suchas RNF168 and FBXW7, by assisting the functionality of thesegenomic alterations. DNA damage response-related E3 ligases,such as RNF168, FBXW7, and HERC2, were generated with morethan 10% mutation in several cancer cells. This study providesa broad list of candidate genes as potential biomarkers for genomicinstability and novel therapeutic targets in cancer. As aDSB related proteins considerably appear the possibilities fortargeting DNA repair defective tumors or hyperactive DNA repairtumors. Based on recent research, we describe the relationshipbetween unstable DSB repairs and DSB-related E3 ligases.
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