Recent studies have revealed that
rottlerin is a natural chemical drug to exert its anti-
cancer activity. However, the molecular mechanisms of
rottlerin-induced
tumor suppressive function have not been fully elucidated. Notch signaling pathway has been characterized to play a crucial role in
tumorigenesis. Therefore, regulation of Notch pathway could be beneficial for the treatment of human
cancer. The aims of our current study were to explore whether
rottlerin could suppress Notch-1 expression, which leads to inhibition of cell proliferation, migration and invasion in
nasopharyngeal carcinoma cells. We performed several approaches, such as CTG, Flow cytometry, scratch healing assay, transwell and Western blotting. Our results showed that
rottlerin treatment inhibited cell growth, migration and invasion, and triggered apoptosis, and arrested cell cycle to G1 phase. Moreover, the expression of Notch-1 was obvious decreased in
nasopharyngeal carcinoma cells after
rottlerin treatment. Importantly, overexpression of Notch-1 promoted cell growth and invasion, whereas down-regulation of Notch-1 inhibited cell growth and invasion in
nasopharyngeal carcinoma cells. Notably, we found the over-expression of Notch-1 could abrogate the anti-
cancer function induced by
rottlerin. Strikingly, our study implied that Notch-1 could be a useful target of
rottlerin for the prevention and treatment of human
nasopharyngeal carcinoma.