Acetaldehyde induces matrix metalloproteinase-9 gene expression via nuclear factor-κB and activator protein 1 signaling pathways in human hepatocellular carcinoma cells: association with the invasive potential

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 醫學院 > 醫學系 > 期刊論文 > Item 310903500/1995

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题名:	Acetaldehyde induces matrix metalloproteinase-9 gene expression via nuclear factor-κB and activator protein 1 signaling pathways in human hepatocellular carcinoma cells: association with the invasive potential
作者:	項千芸(Chien-Yun Hsiang);吳世祿(Shih-Lu Wu);陳兆群(Jaw-Chyun Chen);羅欣宜(Hsin-Yi Lo);李佳橙(Chia-Cheng Li);江素瑛(Su-yin Chiang);吳琇卿(Wu,Hsiu-Chung);侯庭鏞(Tin-Yun Ho)*
贡献者:	醫學院醫學系學士班微生物學科
关键词:	Acetaldehyde;Matrix metalloproteinase-9;Tumor invasion;Nuclear factor-κB;Activator protein 1
日期:	2007-06
上传时间:	2009-08-19 17:23:33 (UTC+8)
摘要:	Alcohol consumption is a significant risk factor for hepatocellular carcinoma (HCC). Alcohol also increases the prevalence of invasion in HCC patients. However, the molecular mechanism on the metastatic effect of alcohol is unclear so far. Herein we demonstrated that acetaldehyde, the primary metabolite of ethanol, increased matrix metalloproteinase-9 (MMP-9) gelatinolytic activity and promoted cell invasion through the up-regulation of MMP-9 gene transcription in HepG2 cells. The transcription of MMP-9 gene was regulated by 10 μM acetaldehyde via inductions of nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) activities. Acetaldehyde stimulated the translocation of NF-κB into nucleus through inhibitory κB-α (IκB-α) and c-Jun N-terminal kinase (JNK)/β-transducin repeat-containing protein (β-TrCP) signaling pathways. Acetaldehyde also induced AP-1 activity via the phosphorylation of p38 kinase. In conclusion, our findings demonstrated for the first time that acetaldehyde activated NF-κB and AP-1 activities via IκB, JNK/β-TrCP, and p38 signaling pathways, resulting in MMP-9 gene expression and hepatocarcinoma cells invasion. These results suggested that acetaldehyde might be a potential factor involved in the invasiveness of HCC in alcoholic patients.
關聯:	TOXICOLOGY LETTERS 171(1-2):78~86
显示于类别:	[醫學系] 期刊論文

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