The involvement of the hepatitis B virus X(HBx)protein in epigenetic modifications during hepatocarcinogenesis has been previously *** noncodingRNAs(IncRNAs),a kind of epigenetic regulator molecules,have also been sho...
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The involvement of the hepatitis B virus X(HBx)protein in epigenetic modifications during hepatocarcinogenesis has been previously *** noncodingRNAs(IncRNAs),a kind of epigenetic regulator molecules,have also been shown to play crucial roles in HBx-related hepatocellular carcinoma(HCC).In this study,we analyzed the key transcription factors of aberrantly expressed IncRNAs in HBx transgenic mice by bioinformatics prediction,and found that ecotropic viral integration site 1(Evil)was a potential main transcription *** investigation showed that EVI1 was positively correlated to HBx expression and was frequently up-regulated in HBV-related HCC *** forced expression of HBx in liver cell lines resulted in a significant increase of the expression of EVIL Furthermore,suppression of EVI1expression by siRNA decreased the proliferation of HCC cells overexpressing HBx in vitro and in ***:Our findings suggest that EVI1 is frequently up-regulated and regulates a cluster of IncRNAs in HBV-related hepatocellular carcinoma(HCC).These findings highlight a novel mechanism for HBx-induced hepatocarcinogenesis through transcription factor EVI1 and its target IncRNAs,and provide a potential new approach to predict the functions of IncRNAs.
The exact mechanisms of gender disparity in hepatocellular carcinoma(HCC)are largely *** of large-scale genomic profiles lead us to explore the gender differences from copy number variations(CNVs).UBE2D1,one of genes ...
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The exact mechanisms of gender disparity in hepatocellular carcinoma(HCC)are largely *** of large-scale genomic profiles lead us to explore the gender differences from copy number variations(CNVs).UBE2D1,one of genes harbored in the gender associated CNVs,can facilitate the HCC growth by activating the p53 ubiquitination through ***,the gender disparity of CNVs in HCC was ascribed to the continuous IL-6 *** IL-6 stimulation promoted the replication stress response and genomic instability to drive the genomic amplification of UBE2D1 by activating STAT3 and thus repressing *** findings clarified the mechanisms of gender disparity in CNVs and suggested UBE2D1 and RAD51B as potential therapeutic targets for HCC.
As long been known,males are more susceptible to hepatocellular carcinoma(HCC)than females,but the reason still remains *** this study,we found that long noncoding RNA five prime to Xist(Inc-FTX)transcribed from X chr...
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As long been known,males are more susceptible to hepatocellular carcinoma(HCC)than females,but the reason still remains *** this study,we found that long noncoding RNA five prime to Xist(Inc-FTX)transcribed from X chromosome inactivation center is gender related that its expression was higher in female liver than in male,and is down-regulated in human HCC tissues.A series of experiments demonstrated that IncFTX plays a negative role in HCC progress by inhibiting HCC cell proliferation,migration and ***-FTX binds to minichromosome maintenance complex component2(MCM2)and impedes DNA replication in HCC *** the other hand,Inc-FTX represses wnt/β-catenin signaling activity by competitively sponging the miR-374 family and inhibits HCC cell EMT and *** female,high level of Inc-FTX in liver inhibits HCC initiation by repressing MCM2 involved DNA *** after HCC initiation in male,low level of Inc-FTX is bounded by elevated MCM2 protein resulting in increased wnt/β-catenin activity,metastasis capacity,and tumor progress than ***,these findings suggest that tumor suppressor Inc-FTX highly expressed in female is one of the important reasons for HCC gender disparity and may contribute to HCC treatment.
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