Abstract
Tyro3, Axl, and Mertk (TAM) receptors are a subfamily of receptor tyrosine kinases. TAM receptors have been implicated in mediating efferocytosis, regulation of immune cells, secretion of inflammatory factors, and epithelial-to-mesenchymal transition in the tumor microenvironment, thereby serving as a critical player in tumor development and progression. The pro-carcinogenic role of TAM receptors has been widely confirmed, overexpression of TAM receptors is tied to tumor cells growth, metastasis, invasion and treatment resistance. Nonetheless, it is surprising to detect that inhibiting TAM signaling is not all beneficial in the tumor immune microenvironment. The absence of TAM receptors also affects anti-tumor immunity under certain conditions by modulating different immune cells, as the functional diversification of TAM signaling is closely related to tumor immunotherapy. Glioblastoma is the most prevalent and lethal primary brain tumor in adults. Although research regarding the crosstalk between TAM receptors and glioblastoma remains scarce, it appears likely that TAM receptors possess potential anti-tumor effects rather than portraying a total cancer-driving role in the context of glioblastoma. Accordingly, we doubt whether TAM receptors play a double-sided role in glioblastoma, and propose the Janus-faced TAM Hypothesis as a conceptual framework for comprehending the precise underlying mechanisms of TAMs. In this study, we aim to cast a spotlight on the potential multidirectional effects of TAM receptors in glioblastoma and provide a better understanding for TAM receptor-related targeted intervention.2C64QgYHEgD3hgVy3P-XM5Video
Highlights
Glioblastoma (GBM) is the most common and fatal primary brain tumor in adults and has a preference for occuring in men and the elderly
This study demonstrated that an increase in local growth arrestspecific 6 (Gas6) can activate TLR/Gas6/TAM signaling, limiting the secretion of pro-inflammatory factors such as tumor necrosis factor α (TNF-α), CXCL1 and CCL2 and the activation of NF-κB
They can indirectly bind to PtdSer through bridging ligand to mediate efferocytosis, which induces an immunosuppressive environment for tumor survival and growth
Summary
Glioblastoma (GBM) is the most common and fatal primary brain tumor in adults and has a preference for occuring in men and the elderly. GBM accounts for 45.2% of primary malignant brain tumors, with the annual incidence of approximately 3 people per 100,000 person worldwide [1, 2]. GBM develops as a result of a malignant. With newer discoveries and a more in-depth study of cancer immune evasion mechanisms, immunotherapy is appeared to be an effective therapeutic option, in addition to traditional surgery, radiotherapy and chemotherapy [12, 13]. Immunotherapy holds great promise for the treatment of aggressive and malignant GBM, considering that the traditional treatments of GBM are restricted [8, 17, 18]. A myriad of clinical trials concerning GBM immunotherapy have been conducted on a large global scale [19, 20]. No obvious clinical benefit has been observed far [19, 21]
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