Effect of allyl isothiocyanate on NF-[kappa]B signaling in 7,12-dimethylbenzanthracene and N-methyl-N-nitrosourea-induced mammary carcinogenesis

Background Inflammation plays a pivotal role in the process of carcinogenesis and phytochemicals have anti-inflammatory properties gaining more importance in cancer chemoprevention. The present study aimed to investigate the anti-inflammatory effect of allyl isothiocyanate (AITC) on 7,12-dimethylbenz(a)anthracene (DMBA)- and N-methyl-N-nitrosourea (MNU)-induced mammary carcinogenesis in female Sprague-Dawley rats. Methods RT-PCR and western blot analysis showed that inflammatory markers such as NF-[kappa]B p65, TNF-[alpha], and IL-6 were overexpressed in mammary tumor tissues. Histological analysis of tumor tissues shows abnormality in hematoxylin and eosin (H&E) staining and toluidine blue (TB) staining of mast cell content, and lipid accumulation in oil red O staining. Results Administration of AITC (20 mg/kg bw) to carcinogen-injected rats significantly decreased the expression of NF-[kappa]B p65, TNF-[alpha], and IL-6 in mammary tissues. Further, molecular docking study demonstrates the binding of AITC to NF-[kappa]B p65. Remarkably, AITC treatments control the growth of cancer cells as clearly evidenced by histopathological analysis. Staining of mammary tissues for mast cells and lipids indicates that AITC treatment to carcinogen-administrated rats significantly reduced mammary tumorigenesis. Conclusions The result suggests that AITC has anti-inflammatory potential to prevent DMBA- and MNU-induced mammary carcinogenesis in rats.