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The effects of luminescent ruthenium(II) polypyridyl functionalized selenium nanoparticles on bFGF-induced
Dongdong Sun1, Yanan Liu, Qianqian Yu
1Department of Chemistry, Jinan University, Guangzhou 510632, China.
Abstract:
Anti-angiogenesis is an effective strategy for cancer treatment because uncontrolled tumor growth depends on tumor angiogenesis and sufficient blood supply. Thus, blocking angiogenesis could be a strategy to arrest tumor growth. The function and mechanism of luminescent ruthenium-modified selenium nanoparticles (Ru-SeNPs) in angiogenesis have not been elucidated to date. Here, we found that Ru-SeNPs significantly inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, migration and tube formation. Ru-SeNPs was also tested in vivo in the chicken chorioallantoic membrane (CAM) assay and found to inhibit bFGF-treated CAMs development like suramin. Moreover, we showed that Ru-SeNPs inhibited the activations of FGFR1 and its downstream protein kinases, such ErK and AKT. Furthermore, by using fluorescence confocal microscopy and TEM imaging studies, we have demonstrated their cellular uptake and localization within the cytoplasm of HepG2 and HUVEC cells. These findings indicate that Ru-SeNPs inhibits angiogenesis and may be a viable drug candidate in anti-angiogenesis and anticancer therapies.
Insights
Ruthenium-modified selenium nanoparticles (Ru-SeNPs) effectively inhibit angiogenesis by blocking key cellular pathways. These nanoparticles show promise as a novel therapeutic strategy for anti-cancer treatments.
Area of Science:
- Biomedical Engineering
- Nanotechnology
- Cancer Research
Background:
- Tumor growth relies on angiogenesis, making anti-angiogenesis a key cancer treatment strategy.
- The role of luminescent ruthenium-modified selenium nanoparticles (Ru-SeNPs) in angiogenesis remains unclear.
- Understanding nanoparticle mechanisms is crucial for developing targeted cancer therapies.
Purpose of the Study:
- To elucidate the function and mechanism of Ru-SeNPs in angiogenesis.
- To evaluate the anti-angiogenic potential of Ru-SeNPs in vitro and in vivo.
- To explore Ru-SeNPs as a potential anti-cancer therapeutic agent.
Main Methods:
- In vitro assays assessing human umbilical vascular endothelial cell (HUVEC) proliferation, migration, and tube formation.
- In vivo chicken chorioallantoic membrane (CAM) assay to evaluate anti-angiogenic effects.
- Western blotting to analyze the activation of FGFR1, Erk, and AKT signaling pathways.
- Confocal microscopy and Transmission Electron Microscopy (TEM) for cellular uptake and localization studies.
Main Results:
- Ru-SeNPs significantly inhibited HUVEC proliferation, migration, and tube formation.
- In vivo CAM assays demonstrated that Ru-SeNPs inhibit angiogenesis, comparable to suramin.
- Ru-SeNPs were found to inhibit the activation of FGFR1 and its downstream kinases, Erk and AKT.
- Cellular uptake and cytoplasmic localization of Ru-SeNPs were confirmed in HepG2 and HUVEC cells.
Conclusions:
- Ru-SeNPs exhibit significant anti-angiogenic properties.
- The mechanism involves the inhibition of FGFR1 signaling pathways.
- Ru-SeNPs represent a promising candidate for anti-angiogenesis and anticancer therapies.
