Abstract
Background: Liver cancer is a severe incurable disease and causes several thousands of deaths each year. Flavonoids are a class of bioactive compounds possessing anti-cancer activity. Objective: The objective of this study is to investigate the role of Buddleoside, one type of flavonoids, in carcinogenesis of liver cancer. Methods: Cell proliferation was detected by CCK-8 method, while cell invasion was by transwell assay, cell apoptosis by Annexin V/FITC-A staining. Western blotting technology was used to explore the mechanism of Buddleoside in liver cancer. Results: It was demonstrated that buddleoside inhibited cell proliferation in a dose-dependent manner and suppressed cell invasion in liver cancer. The inhibition rates of buddleoside in the invasion of both Huh-7 and Hep3B cells were above 75%. The apoptotic rates in the two cell lines were increased by about 10 folds in buddleoside group. Then, the expression levels of NFκB/p65 and IKK were decreased when IκB increased in buddleoside-treated Huh-7 cells, suggesting the inhibition of NFκB signaling pathway. Moreover, the expression levels of cleaved caspase-3 and Bax were upregulated while HSDL2 decreased in buddleoside group. In contrast, after NFκB/p65 was overexpressed, the expression patterns of these molecules were reversed partially. Consistently, the abilities of cell proliferation and cell invasion were recovered, while cell apoptosis decreased after NFκB/p65 overexpression. Conclusion: Buddleoside inhibits proliferation, and invasion and induces apoptosis in liver cancer by regulating NFκB signaling pathway. This study provides us with new proofs for the possible application of buddleoside in liver cancer therapy.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.