The natural flavonoid glycoside vitexin displays preclinical antitumor activity by suppressing NF-κB signaling in nasopharyngeal carcinoma
Authors Wang W, Cheng H, Gu X, Yin X
Received 26 March 2019
Accepted for publication 7 May 2019
Published 5 June 2019 Volume 2019:12 Pages 4461—4468
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Ms Aruna Narula
Peer reviewer comments 3
Editor who approved publication: Dr Carlos E Vigil
Wenbin Wang, Hongbo Cheng, Xilan Gu, Xiaodong Yin
Department of Otorhinolaryngology, Suzhou Municipal Hospital, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou 215000, People’s Republic of China
Background and objectives: Vitexin is a natural flavonoid glycoside mainly extracted from the leaves of vitex, which has a variety of physiological activities. For example, vitexin has antitumor and anti-inflammation activities, and it can also promote blood circulation in the body. However, the function and mechanism of vitexin in nasopharyngeal carcinoma (NPC) are still unclear.
Materials and methods: Cell Counting Kit-8 assay and cell cycle analysis were performed to examine cell survival in response to vitexin. Immunoblotting was used to analyze relative proteins’ expression. NPC xenograft models were established to assess the effect of vitexin in vivo. The luciferase activity of pNFκB-Luc was analyzed by using Dual-Luciferase Reporter Assay System. Quantitative real-time polymerase chain reaction was performed to detect relative genes’ expression. Kinase activity of IKKβ was analyzed in a cell-free system.
Results: In this study, vitexin was found to display significant antitumor activity in NPC in vitro and in vivo. In NPC cells, vitexin inhibited cell cycle progression in NPC cells and induced the cleavages of PARP and inhibited antiapoptotic proteins’ expression, including Bcl-2 and Mcl1. Further studies indicated that vitexin significantly suppressed the luciferase activity of pNF-κB-Luc and inhibited the activation of NF-κB key regulators, including p65, IκBα and IKKs in NPC cells. Moreover, the kinase activity of IKKβ could be suppressed by vitexin in a cell-free system, and overexpression of CA-IKKβ could attenuate the inhibitory effect of vitexin on p65 phosphorylation.
Conclusion: These results indicated that vitexin displayed antitumor activity by suppressing NF-κB signaling in NPC, which suggested that vitexin could be as a potential drug for the treatment of NPC in the future.
Keywords: vitexin, NF-κB, nasopharyngeal carcinoma, cell apoptosis, target
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