Mechanism and Potential of Senolytics in Tumour Microenvironment

Senescent cells (SnCs) produce stress response and enter a state of proliferation arrest under the action of drug radiotherapy and chemotherapy, and secrete senescence related secretory phenotype (SASP), which can participate in the remodeling of tumor microenvironment (TME) through the secretion of inflammatory factors and cancer-promoting factors. The influence of cell senescence on tumors is complex, which has both tumor inhibitory and tumor promoting effects. This study shows that senescent cells are responsible for the tumor promotion mechanism. Senolytics appears as a drug that selectively clears senescent cells. It induces apoptosis by targeting the upregulated anti-apoptotic pathway in senescent cells (such as the BCL-2 family), thereby reducing the accumulation of senescent cells, inhibiting the negative effects of SASP, and improving the TME. Enhance the efficacy of anti-cancer therapy and explore the adverse effects of Senolytics in the TME, aiming to provide new ideas and strategies for future Senolytics therapy optimization and treatment of cancer.