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Updated: May 12, 2026

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
Published on: November 23, 2014
Regulation of tumor angiogenesis by the microtubule-binding protein CLIP-170
Xiaodong Sun1, Fang Li, Bin Dong
1Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, China.
Abstract:
Angiogenesis, the expansion of preexisting blood vessels, is a complex process required for tumor growth and metastasis. Although current antiangiogenic strategies have shown promising results in several cancer types, identification of additional antiangiogenic targets is required to improve the therapeutic response. Herein, we show that the microtubule-binding protein CLIP-170 (cytoplasmic linker protein of 170 kDa) is highly expressed in breast tumor samples and correlates positively with blood vessel density. Depletion of CLIP-170 significantly impaired vascular endothelial tube formation and sprouting in vitro and inhibited breast tumor growth in mice by decreasing tumor vascularization. Our data further show that CLIP-170 is important for the migration but not the proliferation of vascular endothelial cells. In addition, CLIP-170 promotes the polarization of endothelial cells in response to the angiogenic stimulus. These findings thus demonstrate a critical role for CLIP-170 in tumor angiogenesis and suggest its potential as a novel antiangiogenic target.
Insights
Cytoplasmic linker protein 170 (CLIP-170) is highly expressed in breast tumors and drives angiogenesis. Inhibiting CLIP-170 reduces tumor vascularization and growth, identifying it as a potential antiangiogenic target.
Area of Science:
- Oncology
- Cell Biology
- Vascular Biology
Background:
- Angiogenesis is crucial for tumor growth and metastasis.
- Current antiangiogenic therapies show promise but require novel targets.
- Tumor vascularization is a key factor in cancer progression.
Purpose of the Study:
- To investigate the role of CLIP-170 in tumor angiogenesis.
- To determine if CLIP-170 is a viable antiangiogenic target.
- To elucidate the mechanism by which CLIP-170 influences endothelial cells.
Main Methods:
- Quantitative analysis of CLIP-170 expression in breast tumor samples.
- In vitro assays for endothelial cell tube formation and sprouting.
- In vivo studies using mouse models of breast cancer.
- Assessment of endothelial cell migration, proliferation, and polarization.
Main Results:
- CLIP-170 is highly expressed in breast tumors and correlates with blood vessel density.
- CLIP-170 depletion impairs endothelial cell tube formation and sprouting in vitro.
- Inhibition of CLIP-170 reduces tumor growth and vascularization in mice.
- CLIP-170 is essential for endothelial cell migration and polarization, but not proliferation.
Conclusions:
- CLIP-170 plays a critical role in tumor angiogenesis.
- CLIP-170 is a potential novel therapeutic target for antiangiogenic therapy.
- Targeting CLIP-170 may inhibit breast tumor growth by reducing vascularization.
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