Induction of G0/G1 phase arrest and apoptosis by CRISPR/Cas9-mediated knockout of CDK2 in A375 melanocytes.

Cutaneous melanoma is one of the most common malignant skin tumors, with a continuously increasing incidence. Cyclin-dependent kinase (CDK) 2 is a key regulator of G1-S transition and modulation of G2 progression; however, its role in cancer is a matter of debate. In the present study, a lentivirus expressing single-guide RNA (sgRNA) was constructed to knock out CDK2 using CRISP/Cas9 technology, in order to confirm the role of CDK2 in A375 human melanoma cells. The results demonstrated that CDK2 knockout induced G0/G1 phase arrest and early apoptosis by downregulating the expression of CDK4 and cyclin A2, and by upregulating the expression of cyclin D1. These results suggest that therapeutic strategies designed to target CDK2 using CRISP/Cas9 may improve the treatment outcome of cutaneous melanoma.