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iNOS promotes HBx-induced hepatocellular carcinoma via upregulation of JNK activation.

Abstract：

:Inducible nitric oxide (iNOS) is closely correlated with chronic inflammation in hepatitis B virus X protein (HBx)-induced hepatocellular carcinoma (HCC). However, the molecular mechanisms through which iNOS contribute to hepatocarcinogenesis remain poorly understood. Therefore, we investigated the role of iNOS in signaling pathways underlying HBx-induced liver tumorigenesis. iNOS deletion showed a marked decrease in the hepatic tumor size and stage of HBx transgenic (Tg) mice, indicating a strong contribution of iNOS signaling pathways to hepatocarcinogenesis. In addition, we found that nitric oxide (NO) increased HBx mRNA by recruiting CREB to the CRE site of HBV enhancer in HepG2 cells, suggesting a positive feedback loop between HBx and iNOS signaling pathway. Moreover, iNOS-modulated JNK activation was associated with sustained upregulation of Cyclin D1 in HBxTg mice and HepG2-HBx cells. These results imply that iNOS may play a key role in HBx-associated HCC development. Taken together, our findings demonstrate that iNOS aligns with HBx to promote tumor progression. These findings provide a better understating of the mechanism involving HBx-mediated hepatic tumorigenesis and selective inhibition of iNOS may have therapeutic applications in HBx-associated HCC.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Park YH,Shin HJ,Kim SU,Kim JM,Kim JH,Bang DH,Chang KT,Kim BY,Yu DY

doi

10.1016/j.bbrc.2013.04.071

subject

Has Abstract

pub_date

2013-05-31 00:00:00

pages

244-9

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(13)00725-0

journal_volume

435

pub_type

杂志文章

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