Abstract
During angiogenesis, new vessels emerge from existing endothelial lined vessels to promote the degradation of the vascular basement membrane and remodel the extracellular matrix (ECM), followed by endothelial cell migration, and proliferation and the new generation of matrix components. Matrix metalloproteinases (MMPs) participate in the disruption, tumor neovascularization, and subsequent metastasis while tissue inhibitors of metalloproteinases (TIMPs) downregulate the activity of these MMPs. Then, the angiogenic response can be directly or indirectly mediated by MMPs through the modulation of the balance between pro- and anti-angiogenic factors. This review analyzes recent knowledge on MMPs and their participation in angiogenesis.
Highlights
Epithelial-Mesenchymal Transition (EMT) in Metastasis and MigrationCurrently, cancer research is focused on understanding the functional mechanisms underlying cell transformation and tumor progression that can be used to develop new markers and therapies [1]
Other studies have demonstrated that MT1-Matrix metalloproteinases (MMPs) and membrane type 2 matrix metalloproteinase (MT2-MMP) work cooperatively as pro-invasive factors that directly lead to Snail1-triggered cell participation in cancer angiogenesis and metastasis [149]
MT4-MMP expression correlates with EGFR activation, which triggers an angiogenic switch through its catalytic activity and induces the dissemination of cancer cells by disturbing the vessel integrity of the primary breast tumor and promoting hematogenous but not lymphatic metastasis [152,153,154]
Summary
Epithelial-Mesenchymal Transition (EMT) in Metastasis and MigrationCurrently, cancer research is focused on understanding the functional mechanisms underlying cell transformation and tumor progression that can be used to develop new markers and therapies [1]. The increased expression of MMP-1 in human chondrosarcoma is an important prognostic factor and its function in the spread of tumor cells has been evaluated by silencing assays in which cancer metastasis is impaired but local tumor growth and angiogenesis are enhanced [124]. Decreased expression of VEGF and MMP-9 in medulloblastoma cells that overexpress osteonectin, referred to as Secreted Protein Acidic and Rich in Cysteine (SPARC), leads to decreased angiogenesis and tumor growth, indicating the pro-angiogenic role of MMP-9 in cancer tissues [129].
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