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Targeting Frequent Efferocytosis in Tumor Microenvironment is a New Direction for Cancer Treatment
Gangxing Zhu1, Xinliang Wan1, Wanyin Wu1
1Clinical and Basic Research Team of TCM Prevention and Treatment of NSCLC Department of Oncology Guangdong Provincial Hospital of Chinese Medicine Chinese Medicine Guangdong Laboratory State Key Laboratory of Traditional Chinese Medicine Syndrome Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome State Key Laboratory of Dampness Syndrome of Chinese Medicine The Second Clinical College of Guangzhou University of Chinese Medicine Guangzhou 510120 Guangdong China.
Abstract:
A variety of factors, such as dietary habits, the external environment, and individual genetic differences, can lead to the development of cancer. While chemotherapy and radiotherapy are commonly used for cancer treatment, drug resistance and side effects are prevalent issues. Therefore, there is an urgent need to find new treatment modalities. Studies have shown that radiotherapy and chemotherapy can lead to a significant increase in apoptotic cells (ACs) within the tumor microenvironment (TME). The process of phagocytosis helps maintain homeostasis by engulfing and removing these ACs from the organism promptly, which is referred to as efferocytosis. However, it has been observed that excessive efferocytosis can promote the formation of an immunosuppressive TME, which is detrimental to tumor therapy. Thus, inhibiting efferocytosis to enhance the formation of an immune microenvironment shows promise as a treatment direction for tumors. As researchers gradually uncover the molecular mechanisms of efferocytosis, various small-molecule inhibitors and monoclonal antibodies are actively being assessed in clinical trials. Targeting efferocytosis is anticipated to emerge as a promising approach in tumor treatment. In this review, the intricate steps involved in efferocytosis are explored and the current drugs that targeting this process for cancer treatment are outlined.
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