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RPS3a over-expressed in HBV-associated hepatocellular carcinoma enhances the HBx-induced NF-κB signaling via its novel chaperoning function.
PLoS One. 2011; 6(8):e22258.Plos

Abstract

Hepatitis B virus (HBV) infection is one of the major causes of hepatocellular carcinoma (HCC) development. Hepatitis B virus X protein (HBx) is known to play a key role in the development of hepatocellular carcinoma (HCC). Several cellular proteins have been reported to be over-expressed in HBV-associated HCC tissues, but their role in the HBV-mediated oncogenesis remains largely unknown. Here, we explored the effect of the over-expressed cellular protein, a ribosomal protein S3a (RPS3a), on the HBx-induced NF-κB signaling as a critical step for HCC development. The enhancement of HBx-induced NF-κB signaling by RPS3a was investigated by its ability to translocate NF-κB (p65) into the nucleus and the knock-down analysis of RPS3a. Notably, further study revealed that the enhancement of NF-κB by RPS3a is mediated by its novel chaperoning activity toward physiological HBx. The over-expression of RPS3a significantly increased the solubility of highly aggregation-prone HBx. This chaperoning function of RPS3a for HBx is closely correlated with the enhanced NF-κB activity by RPS3a. In addition, the mutational study of RPS3a showed that its N-terminal domain (1-50 amino acids) is important for the chaperoning function and interaction with HBx. The results suggest that RPS3a, via extra-ribosomal chaperoning function for HBx, contributes to virally induced oncogenesis by enhancing HBx-induced NF-κB signaling pathway.

Authors+Show Affiliations

Department of Biotechnology, College of Life science and Biotechnology, Yonsei University, Seoul, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

21857917

Citation

Lim, Keo-Heun, et al. "RPS3a Over-expressed in HBV-associated Hepatocellular Carcinoma Enhances the HBx-induced NF-κB Signaling Via Its Novel Chaperoning Function." PloS One, vol. 6, no. 8, 2011, pp. e22258.
Lim KH, Kim KH, Choi SI, et al. RPS3a over-expressed in HBV-associated hepatocellular carcinoma enhances the HBx-induced NF-κB signaling via its novel chaperoning function. PLoS ONE. 2011;6(8):e22258.
Lim, K. H., Kim, K. H., Choi, S. I., Park, E. S., Park, S. H., Ryu, K., Park, Y. K., Kwon, S. Y., Yang, S. I., Lee, H. C., Sung, I. K., & Seong, B. L. (2011). RPS3a over-expressed in HBV-associated hepatocellular carcinoma enhances the HBx-induced NF-κB signaling via its novel chaperoning function. PloS One, 6(8), e22258. https://doi.org/10.1371/journal.pone.0022258
Lim KH, et al. RPS3a Over-expressed in HBV-associated Hepatocellular Carcinoma Enhances the HBx-induced NF-κB Signaling Via Its Novel Chaperoning Function. PLoS ONE. 2011;6(8):e22258. PubMed PMID: 21857917.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - RPS3a over-expressed in HBV-associated hepatocellular carcinoma enhances the HBx-induced NF-κB signaling via its novel chaperoning function. AU - Lim,Keo-Heun, AU - Kim,Kyun-Hwan, AU - Choi,Seong Il, AU - Park,Eun-Sook, AU - Park,Seung Hwa, AU - Ryu,Kisun, AU - Park,Yong Kwang, AU - Kwon,So Young, AU - Yang,Sung-Il, AU - Lee,Han Chu, AU - Sung,In-Kyung, AU - Seong,Baik L, Y1 - 2011/08/16/ PY - 2011/03/27/received PY - 2011/06/18/accepted PY - 2011/8/23/entrez PY - 2011/8/23/pubmed PY - 2012/2/16/medline SP - e22258 EP - e22258 JF - PloS one JO - PLoS ONE VL - 6 IS - 8 N2 - Hepatitis B virus (HBV) infection is one of the major causes of hepatocellular carcinoma (HCC) development. Hepatitis B virus X protein (HBx) is known to play a key role in the development of hepatocellular carcinoma (HCC). Several cellular proteins have been reported to be over-expressed in HBV-associated HCC tissues, but their role in the HBV-mediated oncogenesis remains largely unknown. Here, we explored the effect of the over-expressed cellular protein, a ribosomal protein S3a (RPS3a), on the HBx-induced NF-κB signaling as a critical step for HCC development. The enhancement of HBx-induced NF-κB signaling by RPS3a was investigated by its ability to translocate NF-κB (p65) into the nucleus and the knock-down analysis of RPS3a. Notably, further study revealed that the enhancement of NF-κB by RPS3a is mediated by its novel chaperoning activity toward physiological HBx. The over-expression of RPS3a significantly increased the solubility of highly aggregation-prone HBx. This chaperoning function of RPS3a for HBx is closely correlated with the enhanced NF-κB activity by RPS3a. In addition, the mutational study of RPS3a showed that its N-terminal domain (1-50 amino acids) is important for the chaperoning function and interaction with HBx. The results suggest that RPS3a, via extra-ribosomal chaperoning function for HBx, contributes to virally induced oncogenesis by enhancing HBx-induced NF-κB signaling pathway. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/21857917/RPS3a_over_expressed_in_HBV_associated_hepatocellular_carcinoma_enhances_the_HBx_induced_NF_κB_signaling_via_its_novel_chaperoning_function_ L2 - http://dx.plos.org/10.1371/journal.pone.0022258 DB - PRIME DP - Unbound Medicine ER -