Sulforaphane suppresses in vitro and in vivo lung tumorigenesis through downregulation of HDAC activity

BackgroundSulforaphane (SFN), an isothiocyanate isolated from broccoli, has been reported to have chemopreventive activity. However, the effects of SFN on lung cancer have not been investigated. In this study, we investigate the chemopreventive role of SFN through the inhibition of histone deacetylase (HDAC) in two different lung cancer cells by in vitro and in vivo mouse models.MethodsA549 and H1299 lung cancer cells were treated with SFN for 48 h. The HDAC activity, expression of acetylated histones H3 and H4, apoptosis and cell cycles were analyzed by western blot, qRT-PCR and flow cytometry. A549 cells were implanted into the immunocompromised mice for xenografts.ResultsThe results showed that SFN inhibited HDAC activity and increased the levels of acetylated histones H3 and H4 in all two lung cancer cells. Further, SFN induced apoptosis, increased the accumulation of cells at G0/G1 and G2/M and arrest cells at S phase. We also found that a concomitant increase of apoptosis related proteins by SFN administration. More interestingly, SFN suppressed the lung cancer growth in xenograft mouse model.ConclusionIn conclusion, the chemopreventive effect of SFN is associated with inhibition of HDAC activity, thereby attenuating lung cancer growth. Therefore, these findings suggest that SFN may be a therapeutic agent for lung cancer through the inhibition of HDAC.