Deciphering the Immunomodulatory Role of Cyclin-Dependent Kinase 4/6 Inhibitors in the Tumor Microenvironment

Cancer is characterized by persistent cell proliferation driven by aberrant cell cycle regulation and stimulation of cyclin-dependent kinases (CDKs). A very intriguing and potential approach for the development of antitumor medicines is the suppression of CDKs that lead to induction of apoptosis and cell cycle arrest. The shift of the cell cycle from the G0/G1 phase to the S phase, which is characterized by active transcription and synthesis, depends on the development of the cyclin D-CDK4/6 complex. A precise balance between anticancer activity and general toxicity is demonstrated by CDK inhibitors, which can specifically block CDK4/6 and control the cell cycle by reducing the G1 to S phase transition. CDK4/6 inhibitors have recently been reported to exhibit significant cell growth inhibition via modulating the tumour microenvironment in cancerous cells. One significant new understanding is that these inhibitors serve important functions in the interaction among tumour cells and the host immune system in addition to being cytostatic. Herein, we discuss the biological significance of CDK4/6 inhibitors in cancer therapeutics, as well as their biological impact on T cells and other important immune cells. Furthermore, we explore the integration of preclinical findings of these pharmaceuticals' ability to enhance antitumor immunity.

Automated summary

Cancer is characterized by abnormal cell cycle regulation and CDK stimulation, and suppressing CDKs is an intriguing approach for anticancer drug development. CDK inhibitors can block CDK4/6 and control the cell cycle, thus inducing apoptosis and cell cycle arrest. Recent studies have shown that CDK4/6 inhibitors not only inhibit cell growth but also modulate the tumor microenvironment and enhance antitumor immunity by affecting the interaction between tumor cells and the host immune system. This article discusses the biological significance of CDK4/6 inhibitors in cancer therapeutics and their impact on immune cells.