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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
Ecto-5'-nucleotidase (CD73) promotes tumor angiogenesis
Li Wang1, Shaoxian Tang, Yingjian Wang
1Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, No. 138 Yixueyuan Road, Shanghai, 200032, China.
Clinical & Experimental Metastasis
|March 20, 2013
Summary
Ecto-5'-nucleotidase (CD73) promotes tumor angiogenesis by enhancing endothelial cell formation of new blood vessels. Inhibiting CD73 reduces tumor growth and metastasis, highlighting its role in cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Tumor growth, progression, and metastasis rely on angiogenesis.
- Ecto-5'-nucleotidase (CD73) expression and activity are elevated in metastatic carcinomas.
- Previous studies suggest CD73 inhibition decreases tumor angiogenesis.
Purpose of the Study:
- To elucidate the mechanism by which CD73 influences tumor angiogenesis.
- To investigate the role of CD73 in endothelial cell function and tumor vascularization.
Main Methods:
- In vitro assays using CD73(+/+) and CD73(-/-) pulmonary microvascular endothelial cells (PMECs).
- Culture of PMECs in cancer-conditioned medium.
- In vivo studies using CD73(+/+) and CD73(-/-) tumor-bearing mice.
- Assessment of endothelial cell adhesion, migration, and capillary-like structure formation.
Main Results:
- CD73(+/+) PMECs formed more capillary-like structures than CD73(-/-) PMECs, especially in cancer-conditioned medium.
- CD73 decreased endothelial cell adhesion to collagen IV but promoted migration.
- Tumor angiogenesis and size were greater in CD73(+/+) mice compared to CD73(-/-) mice.
Conclusions:
- CD73 promotes endothelial cell-mediated new vessel formation under cancer conditions.
- CD73 facilitates tumor growth and hematogenous metastasis.
- Targeting CD73 may represent a therapeutic strategy for inhibiting tumor angiogenesis and metastasis.
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