Sulforaphene inhibits the progression of osteosarcoma via regulating FSTL1/NF-κB pathway

Abstract

AimsSulforaphene (SFE), a naturally occurring isothiocyanate found in cruciferous vegetables, has attracted increasing attention for its anti-cancer effect in many cancers. Main methodsWe explored the therapeutic effects of SFE in modulating the progression of osteosarcoma. CCK8 assay, colony formation assay, western blot, wounding healing assay and transwell assay were conducted to detect the proliferation, apoptosis, migration and invasion of osteosarcoma cells (U2OS and Saos2) treated with different concentrations of SFE. In addition, tumor xenograft in nude mice is performed to test the effects of SFE in tumorigenesis in vivo. Moreover, the levels of FSTL1 and NF-κB were determined by western blot, and loss of functions of FATL1 and NF-κB were further conducted to evaluate the underlying mechanisms of SFE on osteosarcoma development. Key findingsThe results revealed that SFE inhibited the growth while promoted apoptosis of U2OS and Saos2 cells in a dose-dependent manner. Mechanistically, SFE significantly inhibited the expression of NF-κB and FSTL1. However, the genetic intervention of FSTL1 or pharmacologically inhibiting NF-κB weakened the anti-tumor role of SFE. SignificanceThis study suggested that SFE alleviates the progression of osteosarcoma through modulating the FSTL1/NF-κB pathway.