Psoralidin inhibits osteosarcoma function by down-regulating ITGB1 expression through FAK and PI3K/Akt signaling pathways

Background Psoralea is a medicinal plant of legume, which has been used in many diseases for a long time. Psoralidin (PSO) is the main extract of psoralea, which has antibacterial, anti-tumor, anti-inflammatory, antioxidant and other pharmacological activities. The inhibitory effect of PSO on tumor has been found, but its inhibitory effect on osteosarcoma has not been reported. Therefore, this study aimed to evaluate the inhibitory effect of PSO on osteosarcoma and its underlying molecular mechanism. Materials and Methods Crystal violet assay, CCK8 assay, and EdU stain assay were used to confirm the inhibitory effect of PSO on the proliferation of 143B and MG63 osteosarcoma cells. Wound healing and Transwell assays were conducted to evaluate the effects of PSO on osteosarcoma cell migration and invasion. The cell cycle and apoptosis were observed by flow cytometry. RNA sequencing was performed to determine the possible relevant molecular mechanisms, and protein expression levels were analyzed using Western blot. The inhibitory effect of PSO on osteosarcoma in vivo was analyzed by an orthotopic OS tumor animal model and immunohistochemistry. Results According to crystal violet assay, cck8 assay, and EdU stain assay, PSO inhibited cell proliferation in a concentration-dependent manner. Moreover, PSO inhibited the migration and invasion of the osteosarcoma cells. Flow cytometry analysis showed that PSO induces cell cycle arrest and apoptosis in OS cells. To elucidate the molecular mechanism of PSO, we performed RNA-seq analysis and found that PSO treatment significantly inhibited FAK and PI3K/Akt signaling pathways by down-regulating the expression of ITGB1 in MG63 and 143B cells. Furthermore, we confirmed that PSO restrained osteosarcoma growth In vivo mouse models. Conclusion PSO may play an anti-osteosarcoma role via FAK and PI3K/Akt signaling pathways by down-regulating ITGB1 expression