breaks via the non-homologous end joining (NHEJ) repair pathway (Srivastava et al.). Due to its reported success in impeding cancer cell growth and potential impact on future cancer therapeutics, SCR7 has been closely studied in many recent publications (Hosoya & Miyagawa; John et al.).
·Inhibits NHEJ-dependent DNA repair; this inhibition is reported to enhance precise homology-directed repair (HDR)-dependent CRISPR-Cas9 genome editing (Chu et al.; Maruyama et al.; Pinder et al.). However, these effects are cell type-specific and context-dependent (Song et al.; Xie et al.; Yang et al.; Zhang et al.).
·Activates apoptosis of cancer cells by inhibiting DNA ligase IV to increase the efficacy of DNA double-strand break-inducing therapy (chemo- or radio-therapy) (Srivastava et al.).
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