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HUVEC Tube-formation Assay to Evaluate the Impact of Natural Products on Angiogenesis
Published on: June 24, 2019
Monocarbonyl curcumin analog A2 potently inhibits angiogenesis by inducing ROS-dependent endothelial cell death
Bin Liu1, Liu-Su Cui2, Bo Zhou3
1College of Bioengineering, Henan University of Technology, Zhengzhou, 450001, China.
Abstract:
Excessive and abnormal vessel growth plays a critical role in the pathogenesis of many diseases, such as cancer. Angiogenesis is one of the hallmarks of cancer growth, invasion, and metastasis. Discovery of novel antiangiogenic agents would provide new insights into the mechanisms of angiogenesis, as well as potential drugs for cancer treatment. In the present study, we investigated the antiangiogenic activity of a series of monocarbonyl analogs of curcumin synthesized previously in our lab. We found that curcumin analog A2 displayed the full potential to be developed as a novel antiangiogenic agent. Curcumin analog A2 at and above 20 μM dramatically inhibited the migration and tube formation of human umbilical vein endothelial cells (HUVECs) in vitro, new microvessels sprouting from the rat aortic rings ex vivo and newly formed microvessels in chicken chorioallantoic membranes (CAMs) and Matrigel plus in vivo. We further demonstrated that curcumin analog A2 exerted its antiangiogenic activity mainly through inducing endothelial cell death via elevating NADH/NADPH oxidase-derived ROS. Curcumin analog A2 at the antiangiogenic concentrations also triggered autophagy in HUVECs, but this process is neither a pre-requisite for toxicity, leading to the cell death nor a protective response against the toxicity of curcumin analog A2. In conclusion, we demonstrate for the first time the potent antiangiogenic activity of the monocarbonyl curcumin analog A2, which could serve as a promising potential therapeutic agent for the prevention and treatment angiogenesis-related diseases, such as cancer.
Insights
A novel curcumin analog, A2, effectively inhibits cancer angiogenesis by inducing endothelial cell death. This compound shows promise as a potential therapeutic agent for preventing and treating angiogenesis-related diseases like cancer.
Area of Science:
- Biochemistry
- Molecular Biology
- Cancer Research
Background:
- Abnormal blood vessel growth, or angiogenesis, is crucial in cancer development, invasion, and metastasis.
- Identifying new antiangiogenic agents is vital for understanding angiogenesis and developing cancer treatments.
Purpose of the Study:
- To evaluate the antiangiogenic potential of novel monocarbonyl curcumin analogs.
- To identify specific curcumin analogs with significant antiangiogenic activity.
Main Methods:
- Investigated the antiangiogenic activity of synthesized monocarbonyl curcumin analogs.
- Assessed the effects of curcumin analog A2 on human umbilical vein endothelial cell (HUVEC) migration and tube formation in vitro.
- Evaluated A2's impact on microvessel sprouting in rat aortic rings (ex vivo) and in vivo models (chicken chorioallantoic membranes and Matrigel plugs).
- Determined the mechanism of action, focusing on reactive oxygen species (ROS) generation and autophagy induction.
Main Results:
- Curcumin analog A2 significantly inhibited HUVEC migration and tube formation at concentrations of 20 μM and above.
- A2 suppressed new microvessel formation in ex vivo and in vivo models.
- The antiangiogenic effect of A2 was primarily mediated by inducing endothelial cell death through elevated NADH/NADPH oxidase-derived ROS.
- Autophagy was triggered by A2 but was not essential for its toxicity or a protective response.
Conclusions:
- Monocarbonyl curcumin analog A2 exhibits potent antiangiogenic activity.
- A2 demonstrates potential as a therapeutic agent for angiogenesis-related diseases, including cancer.
- The findings highlight A2 as a promising candidate for further development in cancer therapy.
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