Glioma is the most common primary malignant intracranial tumor in the population, and is often associated with abundant angiogenesis. However, how angiogenesis is regulated during glioma progression is still poorly understood. Data mining of cancer patient database shows that MCPIP1 is positively correlated with VEGFA expression and negatively with survival. In this study, we report that overexpressed MCPIP1 in glioma cells is a boost of angiogenesis. Mechanistically, MCPIP1 upregulates the expression of VEGFA in glioma, and promote the secretion of VEGFA to the surroundings, which could stimulate angiogenesis through ERK pathway. Blocking VEGFA expression and secretion inhibited MCPIP1-mediated angiogenesis and glioma progression in vitro and xenograft models. Angiogenesis is the growth of new capillary blood vessels derived from pre-existing capillaries and post-capillary micro-vein. During tumor angiogenesis, endothelial ducts branch to form vascular rings and new basement membranes. Due to the abnormal structure and function of the neointima in tumor tissue and the imperfect vascular matrix, tumor microvasculature is prone to leakage, allowing tumor cells to penetrate directly into the bloodstream and form metastases in distant compartments, without undergoing a complex invasion process.

There is increasing evidence that benign tumors are characterized by sparse angiogenesis and slow vascular growth, whereas most malignant tumors exhibit intensive angiogenesis and rapid growth. Therefore, angiogenesis has an important impact on the development of tumor metastasis, and inhibiting this process will significantly impede tumor development. Human gliomas are very rich in blood vessels and their growth, proliferation and invasion are dependent on angiogenesis. Vascular epithelial growth factor A (VEGFA) is an inducer of angiogenesis produced by tumor cells, and has important roles in promoting endothelial cell survival, vascular permeability, cell proliferation and migration, cellular phenotype, and neo-vascularization. Microvascular endothelial cells activated by pro-angiogenic factors generated by glioma cells usually undergo migration and mitosis, to form new vascular networks connected to the existing vascular system, in which VEGFA plays a critical role. Neovascularization is a prerequisite for glioma growth. Thus, anti-vascular therapy has potential as a new approach for controlling glioma growth.

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Mishita
Jornal co-ordinator
Journal of Heart and Cardiovascular Research