Role of N6-methyladenosine in tumor neovascularization.

Tumor neovascularization is essential for the growth, invasion, and metastasis of tumors. Recent studies have highlighted the significant role of N6-methyladenosine (mA) modification in regulating these processes. This review explores the mechanisms by which mA influences tumor neovascularization, focusing on its impact on angiogenesis and vasculogenic mimicry (VM). We discuss the roles of mA writers, erasers, and readers in modulating the stability and translation of angiogenic factors like vascular endothelial growth factor (VEGF), and their involvement in key signaling pathways such as PI3K/AKT, MAPK, and Hippo. Additionally, we outline the role of mA in vascular-immune crosstalk. Finally, we discuss the current development of mA inhibitors and their potential applications, along with the contribution of mA to anti-angiogenic therapy resistance. Highlighting the therapeutic potential of targeting mA regulators, this review provides novel insights into anti-angiogenic strategies and underscores the need for further research to fully exploit mA modulation in cancer treatment. By understanding the intricate role of mA in tumor neovascularization, we can develop more effective therapeutic approaches to inhibit tumor growth and overcome treatment resistance. Targeting mA offers a novel approach to interfere with the tumor's ability to manipulate its microenvironment, enhancing the efficacy of existing treatments and providing new avenues for combating cancer progression.