DNA Damage and Its Role in Cancer Therapeutics

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.

Automated summary

DNA damage has both positive and negative effects on cancer cells. It exacerbates gene mutation frequency and cancer risk, but it also makes cancer cells more sensitive to chemotherapy or radiotherapy. Inhibitors targeting key enzymes in the DNA repair pathway can induce synthetic lethality with cancer therapeutics. This study reviews the general pathways involved in DNA repair and potential protein targets for cancer therapeutics.