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Conference Paper: Overexpression of histone methyltransferases SUV39H1 and SUV39H2 in hepatocellular carcinoma

TitleOverexpression of histone methyltransferases SUV39H1 and SUV39H2 in hepatocellular carcinoma
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research
Citation
100th American Association for Cancer Research Annual Meeting, Denver, CO, 18-22 April 2009. In Cancer Research, 2009, v. 69, Abstract no. 4499 How to Cite?
AbstractHepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Although the underlying molecular mechanisms remain elusive, accumulating evidence has revealed that aberrant epigenetic events, such as promoter DNA methylation, play a crucial role in liver carcinogenesis. DNA methylation and histone modifications work very closely in regulating proper chromatin structure and gene expression. However, the role of aberrant histone methylation in HCC has not been fully characterized thus far. Methylation on lysine 9 residue of histone 3 protein is an important epigenetic mark for transcriptional repression and heterochromatin formation. In human, H3K9 methylation is catalyzed by SUV39H1 and SUV39H2, human orthologs of Drosophila transcriptional repressor Su(Var)3-9. In this study, using real-time quantitative RT-PCR, we found that both SUV39H1 and SUV39H2 were frequently overexpressed in primary HCC when compared with their corresponding non-tumorous livers. SUV39H1 and SUV39H2 overexpression was found in 60% and 63% of primary HCC, respectively. Clinicopathologically, overexpression of SUV39H1 and SUV39H2 were both significantly associated with the presence of HCC venous invasion (P = 0.020 and 0.043, respectively), an indicator of HCC metastasis. Consistently, ectopic overexpression of SUV39H1 promoted cell migration and invasion of immortalized liver cell line, suggesting that overexpression of SUV39H1/2 may contribute to HCC metastasis. Furthermore, treatment of Su(Var)3-9 inhibitor, Chaetocin, induced G2/M arrest and apoptosis, and suppressed the growth of HCC cell lines at very low concentrations (at nM levels). Our findings suggest that the overexpression of the SUV39H1 and SUV39H2 may play an important role in human HCC and may be potential targets for epigenetic therapy.
Persistent Identifierhttp://hdl.handle.net/10722/62644
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWong, CMen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-07-13T04:05:50Z-
dc.date.available2010-07-13T04:05:50Z-
dc.date.issued2009en_HK
dc.identifier.citation100th American Association for Cancer Research Annual Meeting, Denver, CO, 18-22 April 2009. In Cancer Research, 2009, v. 69, Abstract no. 4499-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/62644-
dc.description.abstractHepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Although the underlying molecular mechanisms remain elusive, accumulating evidence has revealed that aberrant epigenetic events, such as promoter DNA methylation, play a crucial role in liver carcinogenesis. DNA methylation and histone modifications work very closely in regulating proper chromatin structure and gene expression. However, the role of aberrant histone methylation in HCC has not been fully characterized thus far. Methylation on lysine 9 residue of histone 3 protein is an important epigenetic mark for transcriptional repression and heterochromatin formation. In human, H3K9 methylation is catalyzed by SUV39H1 and SUV39H2, human orthologs of Drosophila transcriptional repressor Su(Var)3-9. In this study, using real-time quantitative RT-PCR, we found that both SUV39H1 and SUV39H2 were frequently overexpressed in primary HCC when compared with their corresponding non-tumorous livers. SUV39H1 and SUV39H2 overexpression was found in 60% and 63% of primary HCC, respectively. Clinicopathologically, overexpression of SUV39H1 and SUV39H2 were both significantly associated with the presence of HCC venous invasion (P = 0.020 and 0.043, respectively), an indicator of HCC metastasis. Consistently, ectopic overexpression of SUV39H1 promoted cell migration and invasion of immortalized liver cell line, suggesting that overexpression of SUV39H1/2 may contribute to HCC metastasis. Furthermore, treatment of Su(Var)3-9 inhibitor, Chaetocin, induced G2/M arrest and apoptosis, and suppressed the growth of HCC cell lines at very low concentrations (at nM levels). Our findings suggest that the overexpression of the SUV39H1 and SUV39H2 may play an important role in human HCC and may be potential targets for epigenetic therapy.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Research-
dc.titleOverexpression of histone methyltransferases SUV39H1 and SUV39H2 in hepatocellular carcinomaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, CM: jackwong@pathology.hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.hkuros155431en_HK

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