Tags

Type your tag names separated by a space and hit enter

Dysregulation of β-catenin by hepatitis B virus X protein in HBV-infected human hepatocellular carcinomas.
Front Med China. 2010 Dec; 4(4):399-411.FM

Abstract

β-catenin is a key molecule involved in both cell-cell adhesion and Wnt signaling pathway. In our study, we found that, in the development of hepatocellular carcinoma (HCC), β-catenin was correlated with hepatitis B virus (HBV) X gene encoded protein, which is essential for HBV infectivity and is a potential cofactor in viral carcinogenesis. The expression levels of wild-type β-catenin and E-cadherin were decreased in HepG2 cells expressing hepatitis B virus X protein (HBx), accompanied by destabilization of adherens junction. Reverse transcriptase PCR (RT-PCR), Northern and Western blot showed that reduction of wild-type β-catenin expression involved degradation of the protein. However, RNA interference (RNAi) and luciferase assay indicated that HBx enhanced β-catenin mediated signaling in HepG2 cells. In addition, immunohistochemical and Western blot analysis of β-catenin revealed that a decrease in the β-catenin protein level was found in 58.3% of HBV-related HCCs versus 19.2% of non-HBV-related tumors. Our data suggest that the expression of HBx contributed to the development of HCC, in part, by repressing the wild-type β-catenin expression and enforcing β-catenin-dependent signaling pathway, thus inducing cellular changes leading to acquisition of metastatic and/or proliferation properties.

Authors+Show Affiliations

International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai, 200438, China.No affiliation info availableNo affiliation info availableNo 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

21107751

Citation

Chen, Lei, et al. "Dysregulation of Β-catenin By Hepatitis B Virus X Protein in HBV-infected Human Hepatocellular Carcinomas." Frontiers of Medicine in China, vol. 4, no. 4, 2010, pp. 399-411.
Chen L, Hu L, Li L, et al. Dysregulation of β-catenin by hepatitis B virus X protein in HBV-infected human hepatocellular carcinomas. Front Med China. 2010;4(4):399-411.
Chen, L., Hu, L., Li, L., Liu, Y., Tu, Q. Q., Chang, Y. X., Yan, H. X., Wu, M. C., & Wang, H. Y. (2010). Dysregulation of β-catenin by hepatitis B virus X protein in HBV-infected human hepatocellular carcinomas. Frontiers of Medicine in China, 4(4), 399-411. https://doi.org/10.1007/s11684-010-0170-y
Chen L, et al. Dysregulation of Β-catenin By Hepatitis B Virus X Protein in HBV-infected Human Hepatocellular Carcinomas. Front Med China. 2010;4(4):399-411. PubMed PMID: 21107751.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dysregulation of β-catenin by hepatitis B virus X protein in HBV-infected human hepatocellular carcinomas. AU - Chen,Lei, AU - Hu,Liang, AU - Li,Liang, AU - Liu,Yuan, AU - Tu,Qian-Qian, AU - Chang,Yan-Xin, AU - Yan,He-Xin, AU - Wu,Meng-Chao, AU - Wang,Hong-Yang, Y1 - 2010/11/23/ PY - 2010/08/19/received PY - 2010/10/04/accepted PY - 2010/11/26/entrez PY - 2010/11/26/pubmed PY - 2011/5/18/medline SP - 399 EP - 411 JF - Frontiers of medicine in China JO - Front Med China VL - 4 IS - 4 N2 - β-catenin is a key molecule involved in both cell-cell adhesion and Wnt signaling pathway. In our study, we found that, in the development of hepatocellular carcinoma (HCC), β-catenin was correlated with hepatitis B virus (HBV) X gene encoded protein, which is essential for HBV infectivity and is a potential cofactor in viral carcinogenesis. The expression levels of wild-type β-catenin and E-cadherin were decreased in HepG2 cells expressing hepatitis B virus X protein (HBx), accompanied by destabilization of adherens junction. Reverse transcriptase PCR (RT-PCR), Northern and Western blot showed that reduction of wild-type β-catenin expression involved degradation of the protein. However, RNA interference (RNAi) and luciferase assay indicated that HBx enhanced β-catenin mediated signaling in HepG2 cells. In addition, immunohistochemical and Western blot analysis of β-catenin revealed that a decrease in the β-catenin protein level was found in 58.3% of HBV-related HCCs versus 19.2% of non-HBV-related tumors. Our data suggest that the expression of HBx contributed to the development of HCC, in part, by repressing the wild-type β-catenin expression and enforcing β-catenin-dependent signaling pathway, thus inducing cellular changes leading to acquisition of metastatic and/or proliferation properties. SN - 1673-7458 UR - https://www.unboundmedicine.com/medline/citation/21107751/Dysregulation_of_β-catenin_by_hepatitis_B_virus_X_protein_in_HBV-infected_human_hepatocellular_carcinomas. L2 - http://www.diseaseinfosearch.org/result/3332 DB - PRIME DP - Unbound Medicine ER -