Targeting angiogenesis has emerged as a promising strategy for cancer treatment. Methylseleninic acid (MSA) is a metabolite of selenium (Se) in animal cells that exhibits anti-oxidative and anti-cancer activities at levels exceeding Se nutritional requirements. However, it remains unclear whether MSA exerts its effects on cancer prevention by influencing angiogenesis within Se nutritional levels. Herein, we demonstrate that MSA inhibited angiogenesis at 2 µM, which falls in the range of moderate Se nutritional status. We found that MSA treatments at 2 µM increased cell adherence, while inhibiting cell migration and tube formation of HUVECs in vitro. Moreover, MSA effectively inhibited the sprouts of mouse aortic rings and neoangiogenesis in chick embryo chorioallantoic membrane. We also found that MSA down-regulated integrin β3 at the levels of mRNA and protein, and disrupted clustering of integrin β3 on the cell surface. Additionally, results showed that MSA inhibited the phosphorylation of AKT, IκBα, and NFκB. Overall, our results suggest that exogenous MSA inhibited angiogenesis at nutritional Se levels not only by down-regulating the expression of integrin β3 but also by disorganizing the clustering of integrin β3, which further inhibited the phosphorylation involving AKT, IκBα, NFκB. These findings provide novel mechanistic insight into the function of MSA for regulating angiogenesis and suggest that MSA could be a potential candidate or adjuvant for anti-tumor therapy in clinical settings.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Chikungunya fever (CHIKF), an acute arboviral disease caused by the chikungunya virus (CHIKV), is characterized by fever, debilitating arthralgia, and systemic inflammation, posing a significant public health burden in endemic regions like Guangdong Province, China. The early immunopathological mechanisms following CHIKV infection remain incompletely understood. This prospective cohort study investigated dysregulated effector T cell responses and inflammatory cytokine profiles in 34 patients with acute CHIKF, compared to 20 healthy controls, during a 2025 outbreak in Guangdong. Flow cytometry and multiplex cytokine analysis revealed significant suppression of key effector populations, including CD3 ⁺ T cells, CD8 ⁺ T cells, and natural killer T (NKT) cells, alongside a marked elevation of pro−inflammatory cytokines IL−1β, IL−6, and IL−8. The degree of T cell dysregulation is closely related to the appearance of clinical symptoms, particularly arthralgia and fever. Furthermore, pre−existing comorbidities and advanced age were associated with more pronounced immune abnormalities. Male patients exhibited a higher risk of inflammatory dysregulation, demonstrated by greater NKT cell depletion and IL−1β upregulation compared to females. Notably, pro−inflammatory cytokine levels strongly correlated with neutrophil counts and systemic inflammatory markers but not with T cell subset alterations, suggesting distinct pathological pathways. These findings delineate a dual immunopathogenic state in acute CHIKV infection, involving concurrent effector T cell suppression and IL-1β-associated inflammatory response, which provides insights into potential biomarkers and therapeutic targets for disease management.