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Constitutive activation of nuclear factor kappaB in hepatocellular carcinoma.
Cancer. 2000 Dec 01; 89(11):2274-81.C

Abstract

BACKGROUND

Nuclear factor kappaB (NF-kappaB) is a transcription factor that plays important roles in cell proliferation and in immunity against viral infections. NF-kappaB is a dimer of Rel proteins that is sequestered in the cytoplasm as an inactive form through interaction with an inhibitory kappaB (IkappaB) protein. When IkappaB is degraded, the NF-kappaB dimer will enter the nucleus to activate the target genes. Chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection may activate NF-kappaB and, thus, may modulate cell apoptosis and may be associated with oncogenesis. The role of NF-kappaB in hepatocellular carcinoma (HCC) has not yet been explored.

METHODS

Immunohistochemical staining to search for active nuclear RelA and nuclear IkappaBalpha proteins were done on formalin fixed liver tissues from 65 patients with HCC and from 9 normal control participants. Nuclear extracts of fresh-frozen tumor and nontumor liver tissues from 37 patients with HCC and from 7 normal controls were tested for NF-kappaB-DNA binding activity by electrophoretic mobility shift assay. The RelA and IkappaBalpha protein expressions were studied by Western blot analysis.

RESULTS

Nuclear NF-kappaB stainings were significantly more abundant in HBV-infected or HCV-infected tumors as well as nontumor parts of HCC compared with normal controls. Nuclear NF-kappaB DNA binding activity and nuclear RelA protein expression were greater in tumor tissue compared with nontumor tissue, whereas cytosolic IkappaBalphs protein expression was generally greater in nontumor tissue compared with tumor tissue.

CONCLUSIONS

Constitutive activation of NF-kappaB was found more frequently in tumor tissue compared with nontumor tissue. It is possible that NF-kappaB overexpression accompanied by dysregulation of IkappaBalpha may play a role in the hepatocarcinogenesis of HBV or HCV infection.

Authors+Show Affiliations

Liver Research Unit, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taipei, Taiwan, Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11147598

Citation

Tai, D I., et al. "Constitutive Activation of Nuclear Factor kappaB in Hepatocellular Carcinoma." Cancer, vol. 89, no. 11, 2000, pp. 2274-81.
Tai DI, Tsai SL, Chang YH, et al. Constitutive activation of nuclear factor kappaB in hepatocellular carcinoma. Cancer. 2000;89(11):2274-81.
Tai, D. I., Tsai, S. L., Chang, Y. H., Huang, S. N., Chen, T. C., Chang, K. S., & Liaw, Y. F. (2000). Constitutive activation of nuclear factor kappaB in hepatocellular carcinoma. Cancer, 89(11), 2274-81.
Tai DI, et al. Constitutive Activation of Nuclear Factor kappaB in Hepatocellular Carcinoma. Cancer. 2000 Dec 1;89(11):2274-81. PubMed PMID: 11147598.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Constitutive activation of nuclear factor kappaB in hepatocellular carcinoma. AU - Tai,D I, AU - Tsai,S L, AU - Chang,Y H, AU - Huang,S N, AU - Chen,T C, AU - Chang,K S, AU - Liaw,Y F, PY - 2001/1/9/pubmed PY - 2001/2/28/medline PY - 2001/1/9/entrez SP - 2274 EP - 81 JF - Cancer JO - Cancer VL - 89 IS - 11 N2 - BACKGROUND: Nuclear factor kappaB (NF-kappaB) is a transcription factor that plays important roles in cell proliferation and in immunity against viral infections. NF-kappaB is a dimer of Rel proteins that is sequestered in the cytoplasm as an inactive form through interaction with an inhibitory kappaB (IkappaB) protein. When IkappaB is degraded, the NF-kappaB dimer will enter the nucleus to activate the target genes. Chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection may activate NF-kappaB and, thus, may modulate cell apoptosis and may be associated with oncogenesis. The role of NF-kappaB in hepatocellular carcinoma (HCC) has not yet been explored. METHODS: Immunohistochemical staining to search for active nuclear RelA and nuclear IkappaBalpha proteins were done on formalin fixed liver tissues from 65 patients with HCC and from 9 normal control participants. Nuclear extracts of fresh-frozen tumor and nontumor liver tissues from 37 patients with HCC and from 7 normal controls were tested for NF-kappaB-DNA binding activity by electrophoretic mobility shift assay. The RelA and IkappaBalpha protein expressions were studied by Western blot analysis. RESULTS: Nuclear NF-kappaB stainings were significantly more abundant in HBV-infected or HCV-infected tumors as well as nontumor parts of HCC compared with normal controls. Nuclear NF-kappaB DNA binding activity and nuclear RelA protein expression were greater in tumor tissue compared with nontumor tissue, whereas cytosolic IkappaBalphs protein expression was generally greater in nontumor tissue compared with tumor tissue. CONCLUSIONS: Constitutive activation of NF-kappaB was found more frequently in tumor tissue compared with nontumor tissue. It is possible that NF-kappaB overexpression accompanied by dysregulation of IkappaBalpha may play a role in the hepatocarcinogenesis of HBV or HCV infection. SN - 0008-543X UR - https://www.unboundmedicine.com/medline/citation/11147598/Constitutive_activation_of_nuclear_factor_kappaB_in_hepatocellular_carcinoma_ L2 - https://medlineplus.gov/livercancer.html DB - PRIME DP - Unbound Medicine ER -