Melanoma brain metastases are associated with high incidence and poor prognosis, with their processes of dissemination, colonization, and growth closely influenced by the brain microenvironment. As one of the major cell types in the brain parenchyma, astrocytes facilitate melanoma brain metastasis through multiple mechanisms. Astrocyte-derived factors such as CXCL10, CCL17, NGF, and NT-3 promote the migration of melanoma cells toward the brain. In addition, astrocytes secrete inflammatory cytokines that enhance tumor cell translocation across the blood-brain barrier, and they further support melanoma cell proliferation in the brain via gap junction formation and secretion of unsaturated fatty acids. A deeper understanding of these mechanisms may provide novel insights into the pathogenesis and targeted therapy of melanoma brain metastasis.

Melanoma is a highly malignant tumor characterized by strong invasiveness and a high propensity for brain metastasis. Astrocytes can suppress antitumor immune responses through multiple pathways, thereby establishing an immunosuppressive microenvironment that supports tumor cell survival and promotes immune evasion of brain metastatic melanoma cells. This article reviewed the molecular mechanisms by which astrocytes facilitated immune evasion in brain metastatic melanoma in recent years, aiming to provide insights for identifying novel biomarkers and therapeutic targets for melanoma brain metastasis.

Melanoma is a highly malignant tumor characterized by a high incidence of brain metastases and poor prognosis. This review summarizes recent advances in understanding the mechanisms underlying melanoma brain metastases. The metastatic process involves genetic mutations, such as BRAF mutations, and dysregulated signaling pathways, including the overactivation of the PI3K/AKT pathway, as well as a variety of complex molecular mechanisms. Moreover, melanoma cells interact intricately with the brain microenvironment, including astrocytes and microglia, during the progression of brain metastases. Elucidating these mechanisms provide valuable insights for developing more effective diagnostic and therapeutic strategies, offering novel perspectives for clinical management.

Melanoma brain metastases are associated with high incidence and poor prognosis, with their processes of dissemination, colonization, and growth closely influenced by the brain microenvironment. As one of the major cell types in the brain parenchyma, astrocytes facilitate melanoma brain metastasis through multiple mechanisms. Astrocyte-derived factors such as CXCL10, CCL17, NGF, and NT-3 promote the migration of melanoma cells toward the brain. In addition, astrocytes secrete inflammatory cytokines that enhance tumor cell translocation across the blood-brain barrier, and they further support melanoma cell proliferation in the brain via gap junction formation and secretion of unsaturated fatty acids. A deeper understanding of these mechanisms may provide novel insights into the pathogenesis and targeted therapy of melanoma brain metastasis.

Melanoma is a highly malignant tumor characterized by strong invasiveness and a high propensity for brain metastasis. Astrocytes can suppress antitumor immune responses through multiple pathways, thereby establishing an immunosuppressive microenvironment that supports tumor cell survival and promotes immune evasion of brain metastatic melanoma cells. This article reviewed the molecular mechanisms by which astrocytes facilitated immune evasion in brain metastatic melanoma in recent years, aiming to provide insights for identifying novel biomarkers and therapeutic targets for melanoma brain metastasis.

Melanoma is a highly malignant tumor characterized by a high incidence of brain metastases and poor prognosis. This review summarizes recent advances in understanding the mechanisms underlying melanoma brain metastases. The metastatic process involves genetic mutations, such as BRAF mutations, and dysregulated signaling pathways, including the overactivation of the PI3K/AKT pathway, as well as a variety of complex molecular mechanisms. Moreover, melanoma cells interact intricately with the brain microenvironment, including astrocytes and microglia, during the progression of brain metastases. Elucidating these mechanisms provide valuable insights for developing more effective diagnostic and therapeutic strategies, offering novel perspectives for clinical management.