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Reduced tumor growth and angiogenesis in endoglin-haploinsufficient mice
Annette Düwel1, Nélida Eleno, Mirjana Jerkic
1Instituto Reina Sofia de Investigación Nefrológica, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, España.
Abstract:
Endoglin is a transforming growth factor-beta(1) (TGF-beta(1)) accessory receptor which is highly expressed in tumor vessels. To study the role of endoglin in tumor growth and angiogenesis we induced a highly vascularized tumor in mice heterozygous for endoglin (Eng+/-) and in their control littermates (Eng+/+) by injecting 10(6) Lewis lung carcinoma (3LL) cells subcutaneously. Nine days after injection, the tumor was removed and weighed. Capillary density (CD31 immunohistochemistry), hemoglobin content and vascular cell adhesion molecule-1 (VCAM-1) expression were used to assess tumor vascularization. Tumor perfusion rate was measured by laser-Doppler technique. Expression of the hypoxia-inducible factor (HIF), endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) were determined by Western blot analysis. The aerobic metabolism and oxygen dependency were inferred from the measurement of ATP in tumoral tissue. Tumor weight, capillary density, hemoglobin and VCAM-1 were reduced by about 30% in Eng+/- compared to Eng+/+ littermates. The protein levels of eNOS and phosphorylated eNOS were significantly reduced in Eng+/- compared to Eng+/+ mice. HIF expression was slightly reduced whereas VEGF level was slightly increased in Eng+/- compared to Eng+/+. Tumor tissue levels of ATP and ADP were similar in both types of mice. These data demonstrate that endoglin plays a major role in tumor neoangiogenesis.
Insights
Endoglin deficiency in mice significantly reduced tumor growth and vascularization, indicating its crucial role in promoting new blood vessel formation in tumors.
Area of Science:
- Oncology
- Molecular Biology
- Vascular Biology
Background:
- Endoglin functions as a transforming growth factor-beta(1) (TGF-beta(1)) accessory receptor.
- Endoglin is highly expressed in tumor vasculature, suggesting a role in tumor angiogenesis.
Purpose of the Study:
- To investigate the role of endoglin in tumor growth and angiogenesis.
- To assess the impact of endoglin deficiency on tumor vascularization and related molecular pathways.
Main Methods:
- Lewis lung carcinoma cells were injected into endoglin-heterozygous (Eng+/-) and wild-type (Eng+/+) mice.
- Tumor weight, capillary density (CD31), hemoglobin content, and VCAM-1 expression were measured.
- Tumor perfusion, HIF, eNOS, VEGF, and ATP levels were analyzed.
Main Results:
- Eng+/- mice exhibited approximately 30% reduction in tumor weight, capillary density, hemoglobin, and VCAM-1.
- Endoglin deficiency led to significantly reduced levels of eNOS and phosphorylated eNOS.
- Hypoxia-inducible factor (HIF) was slightly reduced, while vascular endothelial growth factor (VEGF) was slightly increased in Eng+/- mice.
Conclusions:
- Endoglin plays a critical role in tumor neoangiogenesis.
- Reduced endoglin expression impairs tumor vascularization and growth through modulation of eNOS and other angiogenic factors.
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