Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profiles of NIH3T3 cells stably transfected with the plasmids encoding the wild type PreS/S gene or the nonsense mutant gene (sW182*) of HBV.


ABSTRACT: Background and Aims: Whether hepatitis B virus (HBV) could play a direct role in hepatocarcinogenesis remains uncertain. The 3' end nonsense mutations of HBV PreS/S gene have been found to encode transcriptional transactivation activity, suggesting these mutations may contribute to HBV-associated oncogenesis. Recently, we have identified a potent oncogenic HBV surface (S) gene nonsense mutant sW182*. Results: Gene expression microarray study revealed that sW182* mutant was significantly enriched by gene sets associated with cell cycle regulation, DNA repair, or genome instability. The transforming growth factor-induced (TGFBI) gene was downregulated in the sW182* mutant clones, and irresponsive to TGF- treatment. The level of Cyclin D1, a negatively regulated TGFBI target, was highly elevated in sW182* mutant cells. Exogenous expression of TGFBI alleviated the oncogenic activity of sW182* in mouse xenograft study. In human HBV-related HCC cancerous tissue, expression of TGFBI was downregulated in 25 of the 55 (45%) patients. Conclusions: Dysregulation of transforming growth factor-induced (TGFBI) gene is involved in the oncogenic activity of the sW182* mutant of hepatitis B virus S gene. This has never been described before. NIH3T3 cells were stably transfected with plasmids encoding the wild type PreS/S gene or the nonsense mutant (sW182*) of HBV PreS/S gene. Totoal RNAs were extracted from those stable clones for gene expression microarray analysis using Illumina MouseRef-8 V2 BeadChip.

ORGANISM(S): Mus musculus

SUBMITTER: Shih Sheng Jiang 

PROVIDER: E-GEOD-50180 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dysregulation of the TGFBI gene is involved in the oncogenic activity of the nonsense mutation of hepatitis B virus surface gene sW182*.

Jiang Shih Sheng SS   Huang Shiu-Feng SF   Huang Min-Syuan MS   Chen Yng-Tay YT   Jhong Hsiang-Ju HJ   Chang Il-Chi IC   Chen Ya-Ting YT   Chang Jer-Wei JW   Chen Wen-Ling WL   Lee Wei-Chen WC   Chen Miin-Fu MF   Yeh Chau-Ting CT   Matsuura Isao I  

Biochimica et biophysica acta 20140322 7


The nonsense mutations of the hepatitis B virus (HBV) surface (S) gene have been reported to have oncogenic potential. We have previously identified several transforming nonsense mutations of the HBV S gene from hepatocarcinoma (HCC) patients. Among them, the sW182* mutant (the stop codon for tryptophan 182) showed the most potent oncogenicity in a mouse xenograft model using stably transfected mouse fibroblast cells. This study is aimed at understanding the molecular mechanisms leading to the o  ...[more]

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