Expression of nuclear factor-κB in hepatocellular carcinoma and its relation with the X protein of hepatitis B virus

Guo, Shuangping; Wang, Wenliang; Yuqiang, Zhai; Zhao, Yiling

doi:10.3748/wjg.v7.i3.340

Cited by 32 publications

(18 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because p65 is one of the most common members in NF-κB family, and IκB-α is the most important inhibitor, detection of p65 and IκB-α expression can reflect the state of NF-κB metabolism. In our test, low expression rate of p65 and weakly positive expression of IκB-α represented the nonactive state of NF-κB in non-cancerous tissues, but the activation enhancement of NF-κB in HCC was in accord with the previous reports [23,24] . The expression of IκB-α in HCC and its corresponding liver tissue has not been reported yet.…”

Section: Discussionsupporting

confidence: 79%

Activating mechanism of transcriptor NF-kappaB regulated by hepatitis B virus X protein in hepatocellular carcinoma

Wang¹,

Wang²,

Wu³

et al. 2004

WJG

View full text Add to dashboard Cite

AIM:To investigate the mechanism and significance of NF-κB activation regulated by hepatitis B virus X protein (HBx) in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). METHODS:The expression levels of HBx, p65, IκB-α and ubiquitin were detected by immunohistochemistry in HCC tissue microarrays (TMA) respectively, and IκB-α was detected by Western blot in HCC and corresponding liver tissues. RESULTS:The percentage of informative TMA samples was 98.8% in 186 cases with a total of 367 samples. Compared with corresponding liver tissues (60.0%), the HBx expression was obviously decreased in HBV-associated HCC (47. 9%, u=2.24, P<0.05). On the contrary, the expressions of p65 (20.6% vs 45.3%, u=4.85, P<0.01) and ubiquitin (8.9% vs 59.0%, u=9.68, P<0.01) were notably elevated in HCC. In addition, IκB-α had a tendency to go up. Importantly, positive relativity was observed between HBx and p65 (χ Wang T, Wang Y, Wu MC, Guan XY, Yin ZF. Activating mechanism of transcriptor NF-kappaB regulated by hepatitis B virus X protein in hepatocellular carcinoma.

show abstract

Section: Discussionsupporting

confidence: 79%

Activating mechanism of transcriptor NF-kappaB regulated by hepatitis B virus X protein in hepatocellular carcinoma

Wang¹,

Wang²,

Wu³

et al. 2004

WJG

View full text Add to dashboard Cite

show abstract

“…Unlike other types of cancer, HCC has been found usually preceded by chronic inflammation due to viral infection [34][35][36][37] . Matsuyama et al [11] reported that the frequency of mtDNA mutations was markedly increased in both noncancerous and cancerous liver specimens compared with control liver tissue.…”

Section: Discussionmentioning

confidence: 99%

Nuclear and mitochondrial DNA microsatellite instability in Chinese hepatocellular carcinoma

Fang

Fang²,

Wang³

et al. 2004

WJG

View full text Add to dashboard Cite

AIM:To study the nuclear microsatellite instability (nMSI) at BAT26 and mitochondral microsalellite instability (mtMSI) in the occurrence and development of hepatocellular carcinoma and the relationship between nMSI and mtMSI.METHODS: nMSI was observed with PCR and mtMSI with PCR-SSCP in 52 cases of hepatocellular carcinoma.RESULTS: mtMSI was detected in 11 out of the 52 cases of hepatocellular carcinoma (21.2%). Among the 11 cases of hepatocellular carcinoma with mtMSI, 7 occured in one locus and 4 in 2 loci. The frequency of mtMSI in the 52 cases of hepatocellular carcinoma showed no correlation to sex, age, infection of hepatitis B, liver cirrhosis as well as positive AFP of the patients (P>0.05). In addition, nMSI was detected in 3 out of 52 cases of hepatocellular carcinoma (5.8%) and there was no correlation of the incidence of mtMSI to that of nMSI (P>0.05).CONCLUSION: mtMSI may be involved in the coccurrence and development of hepatocellular carcinoma and it is independent of nMSI.Fang DC, Fang L, Wang RQ, Yang SM. Nuclear and mitochondrial DNA microsatellite instability in Chinese hepatocellular carcinoma.

show abstract

“…It is believed that the products of certain NF-B target genes inhibit apoptosis, regulate cell cycle progression, and govern invasion and metastasis (8 -10). NF-B activation has also been implicated in the development of hepatocellular carcinoma (HCC) related to hepatitis B virus (HBV) infection (11,12).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Nuclear Factor-κB, Urokinase-Type Plasminogen Activator, and HBx and Their Clinicopathological Significance in Hepatocellular Carcinoma

Chan¹,

Yau²,

Jin

et al. 2004

Clinical Cancer Research

View full text Add to dashboard Cite

Purpose: Nuclear factor B (NF-B) signaling pathway is an important regulating pathway in human diseases and cancers. One of its downstream target genes is urokinase plasminogen activator (uPA), which is involved in cancer invasion and metastasis. The purpose of this study was to evaluate NF-B activation, uPA up-regulation, and hepatitis B viral X protein (HBx) expression in human hepatocellular carcinoma (HCC) and to assess their clinicopathological significance.Experimental Design: We evaluated NF-B activation, expression of uPA, and presence of HBx in 32 human HCCs. Their clinicopathological significance was assessed by correlation with the clinicopathological features. Aberrant NF-B signaling pathway and uPA up-regulation mediated by HBx were also analyzed in vitro.Results: We found that NF-B activation and uPA upregulation were frequently (56% and 59%, respectively) observed in HCCs, and particularly in HBx-positive HCCs. NF-B activation and uPA overexpression were closely associated with one another (P < 0.0001). Furthermore, both activation of NF-B and up-regulation of uPA were significantly associated with a more aggressive tumor behavior in terms of venous invasion, direct liver invasion, and absence of tumor encapsulation. In vitro, NF-B activation was induced by HBx transfection in HepG2 cells through inhibitor of nuclear factor-B kinase ␤ (IKK␤). HBx also up-regulated uPA and enhanced cell invasion synergistically with IKK␤.Conclusions: The data indicate that NF-B dysregulation and uPA overexpression may lead to a more aggressive tumor behavior in HCC. In addition, our data suggest that IKK␤ plays a critical role in the HBx-activated NF-B signaling pathway.

show abstract

Expression of nuclear factor-κB in hepatocellular carcinoma and its relation with the X protein of hepatitis B virus

Cited by 32 publications

References 44 publications

Activating mechanism of transcriptor NF-kappaB regulated by hepatitis B virus X protein in hepatocellular carcinoma

Activating mechanism of transcriptor NF-kappaB regulated by hepatitis B virus X protein in hepatocellular carcinoma

Nuclear and mitochondrial DNA microsatellite instability in Chinese hepatocellular carcinoma

Evaluation of Nuclear Factor-κB, Urokinase-Type Plasminogen Activator, and HBx and Their Clinicopathological Significance in Hepatocellular Carcinoma

Contact Info

Product

Resources

About