VEGF/VEGFR axis and its signaling in melanoma: Current knowledge toward therapeutic targeting agents and future perspectives

血管内皮生长因子受体 血管生成 黑色素瘤 MAPK/ERK通路 转移 蛋白激酶B PI3K/AKT/mTOR通路 癌症研究 医学 靶向治疗 信号转导 血管内皮生长因子 细胞迁移 免疫学 癌症 细胞 内科学 生物 细胞生物学 遗传学
作者
Mohammad Malekan,Nikolas K. Haass,Ghasem Rahmatpour Rokni,Nasim Gholizadeh,Mohammad Ali Ebrahimzadeh,Armaghan Kazeminejad
出处
期刊:Life Sciences [Elsevier BV]
卷期号:345: 122563-122563 被引量:17
标识
DOI:10.1016/j.lfs.2024.122563
摘要

Melanoma is responsible for most skin cancer-associated deaths globally. The progression of melanoma is influenced by a number of pathogenic processes. Understanding the VEGF/VEGFR axis, which includes VEGF-A, PlGF, VEGF-B, VEGF-C, and VEGF-D and their receptors, VEGFR-1, VEGFR-2, and VEGFR-3, is of great importance in melanoma due to its crucial role in angiogenesis. This axis generates multifactorial and complex cellular signaling, engaging the MAPK/ERK, PI3K/AKT, PKC, PLC-γ, and FAK signaling pathways. Melanoma cell growth and proliferation, migration and metastasis, survival, and acquired resistance to therapy are influenced by this axis. The VEGF/VEGFR axis was extensively examined for their potential as diagnostic/prognostic biomarkers in melanoma patients and results showed that VEGF overexpression can be associated with unfavorable prognosis, higher level of tumor invasion and poor response to therapy. MicroRNAs linking to the VEGF/VEGFR axis were identified and, in this review, divided into two categories according to their functions, some of them promote melanoma angiogenesis (promotive group) and some restrict melanoma angiogenesis (protective group). In addition, the approach of treating melanoma by targeting the VEGF/VEGFR axis has garnered significant interest among researchers. These agents can be divided into two main groups: anti-VEGF and VEGFR inhibitors. These therapeutic options may be a prominent step along with the modern targeting and immune therapies for better coverage of pathological processes leading to melanoma progression and therapy resistance.
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