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Updated: Jul 15, 2026

Isolation and Culture Expansion of Tumor-specific Endothelial Cells
Published on: October 14, 2015
Tumor vesicle-associated CD147 modulates the angiogenic capability of endothelial cells
Danilo Millimaggi1, Marianna Mari, Sandra D'Ascenzo
1Department of Experimental Medicine, L'Aquila University, L'Aquila, Italy.
Abstract:
Matrix metalloproteinase (MMP) degradation of extracellular matrix is thought to play an important role in invasion, angiogenesis, tumor growth, and metastasis. Several studies have demonstrated that CD147/extracellular MMP inducer, a membrane-spanning molecule highly expressed in tumor cells, may be involved in the progression of malignancies by regulating expression of MMP in peritumoral stromal cells. In the present study we show that CD147 is expressed in microvesicles derived from epithelial ovarian cancer cells and that CD147-positive vesicles may promote an angiogenic phenotype in endothelial cells in vitro. Vesicles shed by human ovarian carcinoma cell lines OVCAR3, SKOV3, and A2780 expressed different levels of CD147 and stimulated proangiogenic activities of human umbilical vein endothelial cells (HUVECs) in a CD147-dependent fashion (OVCAR3 > SKOV3 > A2780). Moreover, vesicles shed by ovarian carcinoma cell line CABA I with low CD147 expression had no significant effect on the development of angiogenic phenotype in HUVECs. The treatment of OVCAR3 cells with small interfering RNA against CD147 suppressed the angiogenic potential of OVCAR3-derived microvesicles. However, transfection of CD147 cDNA into the CABA I cell line enabled CABA I-derived vesicles to induce angiogenesis and to promote MMP genes expression in HUVECs. We therefore conclude that vesicles shed by ovarian cancer cells may induce proangiogenic activities of HUVECs by a CD147-mediated mechanism.
Insights
Ovarian cancer cells release microvesicles containing CD147, a molecule that promotes blood vessel growth (angiogenesis) in endothelial cells. This CD147-mediated mechanism in microvesicles contributes to ovarian cancer progression.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Matrix metalloproteinases (MMPs) are crucial for tumor invasion, angiogenesis, growth, and metastasis.
- CD147, a transmembrane molecule highly expressed in tumor cells, regulates MMP expression in stromal cells, potentially driving cancer progression.
Purpose of the Study:
- To investigate the role of CD147 in microvesicles shed by ovarian cancer cells.
- To determine if these CD147-positive microvesicles promote angiogenesis in endothelial cells.
Main Methods:
- Analyzing CD147 expression in microvesicles from ovarian carcinoma cell lines (OVCAR3, SKOV3, A2780, CABA I).
- Assessing the proangiogenic effects of these microvesicles on human umbilical vein endothelial cells (HUVECs).
- Utilizing small interfering RNA (siRNA) to downregulate CD147 in OVCAR3 cells and transfecting CD147 cDNA into CABA I cells.
Main Results:
- Microvesicles from ovarian cancer cells (OVCAR3, SKOV3, A2780) expressed varying levels of CD147 and promoted HUVEC angiogenesis in a CD147-dependent manner.
- Microvesicles from CABA I cells with low CD147 expression showed no significant angiogenic effect.
- siRNA-mediated CD147 knockdown in OVCAR3 cells reduced the angiogenic potential of their microvesicles.
- CD147 transfection into CABA I cells rendered their microvesicles angiogenic and capable of promoting MMP gene expression in HUVECs.
Conclusions:
- Microvesicles shed by ovarian cancer cells can induce proangiogenic activities in endothelial cells.
- This proangiogenic effect is mediated by CD147 expressed on these microvesicles.
- CD147-positive microvesicles represent a novel mechanism by which ovarian cancer promotes angiogenesis and potentially contributes to tumor progression.
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