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Abstract Cyclin-dependent kinase 4/6 (CDK4/6) acts as a crucial point of regulation in the G1-to-S transition in the cell division cycle, its aberrant activation was found in various human cancers, leading to abnormal cell proliferation. Recent clinical trials have reported that combined with other small-molecule targeted therapies, CDK4/6 inhibitors increase overall survival and objective response rates in breast cancer (BC), non-small cell lung cancer (NSCLC), and head and neck squamous cell carcinoma (HNSCC). Notably, targeting CDK4/6 triggers an antitumor immune response, providing a potential combined application method for immunotherapy. In this review, we summarize underlying mechanism of targeting CDK4/6 in regulating antigen presentation, immune cell activation, and tumor immune microenvironment (TIME) remodeling and in producing synergistic effects with immune checkpoint blockade (ICB) in cancer clinical treatment.
Sun et al. (Thu,) studied this question.