DNA Damage and Its Role in Cancer Therapeutics

被引：41

作者：

Moon, Jaeyoung ^{[1
]}

Kitty, Ichiwa ^{[1
]}

Renata, Kusuma ^{[1
,2
]}

Qin, Sisi ^{[3
]}

Zhao, Fei ^{[4
]}

Kim, Wootae ^{[1
]}

机构：

[1] Soonchunhyang Univ, Soonchunhyang Inst Med bio Sci SIMS, Dept Integrated Biomed Sci, Cheonan 31151, Chungcheongnam, South Korea

[2] Atma Jaya Catholic Univ Indonesia, Biotechnol, Jakarta 12930, Indonesia

[3] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA

[4] Hunan Univ, Coll Biol, Changsha 410082, Peoples R China

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2023年 / 24卷 / 05期

基金：

新加坡国家研究基金会;

关键词：

DNA damage; cancer therapeutics; mutations; STRAND BREAK REPAIR; BASE EXCISION-REPAIR; MISMATCH-REPAIR; SYNTHETIC LETHALITY; HOMOLOGOUS RECOMBINATION; CHROMOSOMAL REARRANGEMENTS; COLORECTAL-CANCER; LIGASE INHIBITORS; PARP INHIBITION; END RESECTION;

D O I：

10.3390/ijms24054741

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

DNA damage is a double-edged sword in cancer cells. On the one hand, DNA damage exacerbates gene mutation frequency and cancer risk. Mutations in key DNA repair genes, such as breast cancer 1 (BRCA1) and/or breast cancer 2 (BRCA2), induce genomic instability and promote tumorigenesis. On the other hand, the induction of DNA damage using chemical reagents or radiation kills cancer cells effectively. Cancer-burdening mutations in key DNA repair-related genes imply relatively high sensitivity to chemotherapy or radiotherapy because of reduced DNA repair efficiency. Therefore, designing specific inhibitors targeting key enzymes in the DNA repair pathway is an effective way to induce synthetic lethality with chemotherapy or radiotherapy in cancer therapeutics. This study reviews the general pathways involved in DNA repair in cancer cells and the potential proteins that could be targeted for cancer therapeutics.

引用

页数：19

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