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The twisted survivin connection to angiogenesis
C Sanhueza1, S Wehinger2, J Castillo Bennett3,4
1Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, 8330024, Chile.
Abstract:
Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.
Insights
Survivin protein overexpression in cancer cells drives tumor angiogenesis by promoting VEGF synthesis and secretion. This involves a feedback loop enhancing tumor vascularization and growth.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Survivin, an inhibitor of apoptosis protein (IAP), is overexpressed in most human cancers.
- Its role in cell division, apoptosis, metastasis, and angiogenesis makes it a potential cancer treatment target.
Purpose of the Study:
- To discuss recent findings on survivin expression regulation and its role in angiogenesis, especially under hypoxia.
- To propose a novel role for survivin in promoting VEGF synthesis, secretion, and angiogenesis in cancer cells.
Main Methods:
- Review of recent findings on survivin regulation and function.
- Mechanistic proposal involving PI3-kinase/Akt and β-Catenin-TCF/LEF pathways.
- Discussion of survivin's contribution to tumor vascularization.
Main Results:
- Survivin expression in tumor cells promotes VEGF synthesis and secretion.
- A positive feedback loop involving PI3-kinase/Akt activation enhances VEGF expression.
- This mechanism contributes to tumor vascularization via angiogenesis and vasculogenic mimicry.
Conclusions:
- Survivin plays a novel role in promoting tumor angiogenesis through VEGF.
- A PI3-kinase/Akt and β-Catenin-TCF/LEF dependent feedback loop regulates VEGF expression.
- Survivin-mediated mechanisms enhance tumor vascularization, impacting cancer progression.
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