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Conference Paper: The functional role of a putative tumor suppressor protein, TAX1 binding protein 2(TAX1BP2) in hepatocellular carcinoma

TitleThe functional role of a putative tumor suppressor protein, TAX1 binding protein 2(TAX1BP2) in hepatocellular carcinoma
Other TitlesThe function role of a putative tumor suppressor protein, TAX1 binding protein 2 in HCC
Authors
Issue Date2015
PublisherThe University of Hong Kong.
Citation
The State Key Laboratory For Liver Research Sympsium 2015: From Bench Research to Patient Care, Hong Kong, 17 October 2015 How to Cite?
AbstractTAX1 binding protein 2 (TAX1BP2), which is a centrosomal protein, is first identified as a cellular interacting partner of human T-cell leukemia virus I (HTLV-I) encoded oncoprotein, TAX. Recently, TAX1BP2 was found to frequently underexpress in hepatocellular carcinoma (HCC) and underexpression of TAX1BP2 suppressed the level of an important tumor suppressor, p53 in a p38 MAPK dependent manner, strongly suggesting that TAX1BP2 is a putative tumor suppressor in HCC. TAX1BP2 is also involved in the chemo-sensitivity of HCC cells. We observed that the level of TAX1BP2 was significantly induced in HCC cells treated with the chemotherapeutic drugs, Cisplatin and Etoposide. To understand the role of TAX1BP2 in chemo-resistance, we demonstrated that TAX1BP2 was a phosphorylation substrate of a major DNA damage response kinase, called ATM and the phosphorylation of TAX1BP2 by ATM significantly modulated the protein level of TAX1BP2 via ubiquitination proteasomal degradation. In addition to the regulation by DNA damage response, we found that TAX1BP2 was also downregulated in cancer stem cell marker, CD133 positive cells, suggesting that TAX1BP2 may act downstream of CD133 signaling to regulate the chemo-sensitivity of HCC.
DescriptionBasic Research Presentation
Persistent Identifierhttp://hdl.handle.net/10722/233966

 

DC FieldValueLanguage
dc.contributor.authorChing, YP-
dc.date.accessioned2016-10-14T02:53:21Z-
dc.date.available2016-10-14T02:53:21Z-
dc.date.issued2015-
dc.identifier.citationThe State Key Laboratory For Liver Research Sympsium 2015: From Bench Research to Patient Care, Hong Kong, 17 October 2015-
dc.identifier.urihttp://hdl.handle.net/10722/233966-
dc.descriptionBasic Research Presentation-
dc.description.abstractTAX1 binding protein 2 (TAX1BP2), which is a centrosomal protein, is first identified as a cellular interacting partner of human T-cell leukemia virus I (HTLV-I) encoded oncoprotein, TAX. Recently, TAX1BP2 was found to frequently underexpress in hepatocellular carcinoma (HCC) and underexpression of TAX1BP2 suppressed the level of an important tumor suppressor, p53 in a p38 MAPK dependent manner, strongly suggesting that TAX1BP2 is a putative tumor suppressor in HCC. TAX1BP2 is also involved in the chemo-sensitivity of HCC cells. We observed that the level of TAX1BP2 was significantly induced in HCC cells treated with the chemotherapeutic drugs, Cisplatin and Etoposide. To understand the role of TAX1BP2 in chemo-resistance, we demonstrated that TAX1BP2 was a phosphorylation substrate of a major DNA damage response kinase, called ATM and the phosphorylation of TAX1BP2 by ATM significantly modulated the protein level of TAX1BP2 via ubiquitination proteasomal degradation. In addition to the regulation by DNA damage response, we found that TAX1BP2 was also downregulated in cancer stem cell marker, CD133 positive cells, suggesting that TAX1BP2 may act downstream of CD133 signaling to regulate the chemo-sensitivity of HCC.-
dc.languageeng-
dc.publisherThe University of Hong Kong.-
dc.relation.ispartofState Key Laboratory for Liver Research Symposium 2015-
dc.titleThe functional role of a putative tumor suppressor protein, TAX1 binding protein 2(TAX1BP2) in hepatocellular carcinoma-
dc.title.alternativeThe function role of a putative tumor suppressor protein, TAX1 binding protein 2 in HCC-
dc.typeConference_Paper-
dc.identifier.emailChing, YP: ypching@hku.hk-
dc.identifier.authorityChing, YP=rp00469-
dc.identifier.hkuros267242-
dc.publisher.placeHong Kong-

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