Abstract
Objective Neuroblastoma (NB) is a highly metastatic tumor in children that develops in the sympathetic nervous system and has a low curative rate. Saikosaponin A (SSA), an active ingredient isolated from the root of Radix Bupleuri, is a natural compound with various pharmacological activities and shows good application prospects in antitumors. This study investigated the antihuman NB activity of SSA and underlying mechanisms associated with its actions. Materials and Methods The MTT method was used to detect the activity of SSA in inhibiting human NB cell SK-N-AS proliferation. Cell morphology was observed. The flow cytometry technology was used in analyzing the cell apoptosis rate. The Transwell assay evaluated cell migration and invasion following SSA treatment, apoptosis-related protein expression, and angiogenesis-related protein expression, and EMT-related proteins were detected by western blot analysis. Results SSA showed an inhibitory effect on SK-N-AS cells with the IC50 values of 14.14 μM at 24 h and 12.41 μM at 48 h. Results indicated that SSA has proapoptotic activity, and its proapoptotic activity is positively correlated with the Bax/Bcl-2/caspase-9/caspase-7/PARP pathway. Furthermore, SSA inhibited the invasion and migration of SK-N-AS cells via regulating the angiogenesis-related VEGFR2/Src/Akt pathway and the epithelial-mesenchymal transition- (EMT-) related protein expression. Conclusion SSA exerts an antihuman NB effect and thus provides foundations for NB treatment.
Highlights
Neuroblastoma (NB) as a malignant tumor is a common pediatric extracranial solid tumor that develops from the sympathoadrenal lineage derived from the neural crest [1,2,3]
The results showed that Saikosaponin A (SSA) had little cytotoxicity on normal human cells
The experimental concentrations for the detection of invasion and migration were 7.5, 10, or 12.5 μM
Summary
Neuroblastoma (NB) as a malignant tumor is a common pediatric extracranial solid tumor that develops from the sympathoadrenal lineage derived from the neural crest [1,2,3]. A substantial number of survivors continue to experience many long-term side effects and develop various chronic health-related complications, and tumors frequently show resistance to any therapy after relapsing [6, 7]. Older patients with metastatic disease have an approximately 50% event-free survival despite aggressive multimodal therapies with long-term severe side effects [8, 9]. It is of great clinical and scientific significance that novel therapeutic agents associated with NB be identified. MYCN-amplified NB and non-MYCN-amplified NB are two subtypes of NB cells. The previous studies showed that the overexpression of the MYCN gene is a leading cause of NB [11].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
