NDLI: Vanillin inhibits matrix metalloproteinase-9 expression through down-regulation of nuclear factor-kappaB signaling pathway in human hepatocellular carcinoma cells.

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Vanillin inhibits matrix metalloproteinase-9 expression through down-regulation of nuclear factor-kappaB signaling pathway in human hepatocellular carcinoma cells.

Content Provider	Semantic Scholar
Author	Liang, Ji-An Wu, Shih-Lu Lo, Hsin-Yi Hsiang, Chien-Yun Ho, Tin-Yun
Copyright Year	2009
Abstract	Vanillin has been reported to exhibit anti-invasive and antimetastatic activities by suppressing the enzymatic activity of matrix metalloproteinase-9 (MMP-9). However, the underlying mechanism of anti-invasive activity remains unclear so far. Herein we demonstrate that vanillin reduced 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced MMP-9 gelatinolytic activity and suppressed cell invasion through the down-regulation of MMP-9 gene transcription in HepG2 cells. Vanillin significantly reduced the 6.6-fold invasive capacity of HepG2 cells in noncytotoxic concentrations, and this anti-invasive effect was concentration-dependent in the Matrigel invasion assay. Moreover, vanillin significantly suppressed the TPA-induced enzymatic activity of MMP-9 and decreased the induced mRNA level of MMP-9. Analysis of the transcriptional regulation indicated that vanillin suppressed MMP-9 transcription by inhibiting nuclear factor-kappaB (NF-kappaB) activity. Western blot further confirmed that vanillin inhibited NF-kappaB activity through the inhibition of IkappaB-alpha phosphorylation and degradation. In conclusion, vanillin might be a potent antiinvasive agent that suppresses the MMP-9 enzymatic activity via NF-kappaB signaling pathway.
File Format	PDF HTM / HTML
DOI	10.1124/mol.108.049502
PubMed reference number	18835982
Journal	Medline
Volume Number	75
Issue Number	1
Alternate Webpage(s)	http://molpharm.aspetjournals.org/content/molpharm/75/1/151.full.pdf
Alternate Webpage(s)	https://doi.org/10.1124/mol.108.049502
Journal	Molecular pharmacology
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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