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Conference Paper: Combination of HDAC and proteasome inhibitors up-regulates P16INK4A and P21WAF1 and induces apoptosis of EBV-Transformed lymphoblastoid cell lines

TitleCombination of HDAC and proteasome inhibitors up-regulates P16INK4A and P21WAF1 and induces apoptosis of EBV-Transformed lymphoblastoid cell lines
Authors
KeywordsPediatrics
Issue Date2015
PublisherMedcom Limited. The Journal's web site is located at http://www.hkjpaed.org/index.asp
Citation
The 2014 Joint Annual Scientific Meeting of the Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association, Hong Kong, 15 June 2014. In Hong Kong Journal of Paediatrics, 2014, v. 19 n. 3, p. 205 How to Cite?
AbstractEpstein-Barr virus (EBV) transforms B cells through its unique set of latent genes into continually proliferating lymphoblastoid cell lines (LCLs). Amongst the latent genes, EBV nuclear antigen (EBNA)-3A and -3C exert antiapoptotic effects on the LCLs through down-regulation of p16INK4A and p21WAF1. Histone deacetylase (HDAC) inhibitors induce apoptosis of various types of cancer cells through up-regulation of p16INK4A and p21WAF1 and proteasome inhibitors can enhance the anti-tumour effect of HDAC inhibitors through the generation of reactive oxygen species (ROS). Here, we hypothesise that combination of HDAC and proteasome inhibitors can counteract the anti-apoptotic effects of EBNA-3A and -3C in LCLs. We found that combination of HDAC (SAHA or romidepsin) and proteasome inhibitors (bortezomib or carfilzomib) could synergistically inhibit cell proliferation and mediate apoptosis, as evidenced by the annexin V-positive and sub-G1 populations as well as proteolytic cleavage of PARP and caspase-3, in three LCLs. The drug combinations did not affect the expression level of EBNA-3A and -3C whereas they directly induced the expression of p16INK4A and p21WAF1. Both up-regulation of p16INK4A and p21WAF1 and induction of apoptosis were dependent on the generation of ROS. We conclude that combination of HDAC and proteasome inhibitors may counteract the anti-apoptotic effects of EBNA-3A and -3C by the up-regulation of p16INK4A and p21WAF1, thereby inducing apoptosis of EBVtransformed LCLs.
DescriptionPoster Presentation
This journal issue (pp. 192-206) entitled: Proceedings of Congress: Joint Annual Scientific Meeting 2014: The Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association 15 June, 2014
Open Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/209590
ISSN
2015 Impact Factor: 0.194
2015 SCImago Journal Rankings: 0.123

 

DC FieldValueLanguage
dc.contributor.authorYeung, PL-
dc.contributor.authorHui, KF-
dc.contributor.authorLeung, YY-
dc.contributor.authorChiang, AKS-
dc.date.accessioned2015-05-05T03:06:03Z-
dc.date.available2015-05-05T03:06:03Z-
dc.date.issued2015-
dc.identifier.citationThe 2014 Joint Annual Scientific Meeting of the Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association, Hong Kong, 15 June 2014. In Hong Kong Journal of Paediatrics, 2014, v. 19 n. 3, p. 205-
dc.identifier.issn1013-9923-
dc.identifier.urihttp://hdl.handle.net/10722/209590-
dc.descriptionPoster Presentation-
dc.descriptionThis journal issue (pp. 192-206) entitled: Proceedings of Congress: Joint Annual Scientific Meeting 2014: The Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association 15 June, 2014-
dc.descriptionOpen Access Journal-
dc.description.abstractEpstein-Barr virus (EBV) transforms B cells through its unique set of latent genes into continually proliferating lymphoblastoid cell lines (LCLs). Amongst the latent genes, EBV nuclear antigen (EBNA)-3A and -3C exert antiapoptotic effects on the LCLs through down-regulation of p16INK4A and p21WAF1. Histone deacetylase (HDAC) inhibitors induce apoptosis of various types of cancer cells through up-regulation of p16INK4A and p21WAF1 and proteasome inhibitors can enhance the anti-tumour effect of HDAC inhibitors through the generation of reactive oxygen species (ROS). Here, we hypothesise that combination of HDAC and proteasome inhibitors can counteract the anti-apoptotic effects of EBNA-3A and -3C in LCLs. We found that combination of HDAC (SAHA or romidepsin) and proteasome inhibitors (bortezomib or carfilzomib) could synergistically inhibit cell proliferation and mediate apoptosis, as evidenced by the annexin V-positive and sub-G1 populations as well as proteolytic cleavage of PARP and caspase-3, in three LCLs. The drug combinations did not affect the expression level of EBNA-3A and -3C whereas they directly induced the expression of p16INK4A and p21WAF1. Both up-regulation of p16INK4A and p21WAF1 and induction of apoptosis were dependent on the generation of ROS. We conclude that combination of HDAC and proteasome inhibitors may counteract the anti-apoptotic effects of EBNA-3A and -3C by the up-regulation of p16INK4A and p21WAF1, thereby inducing apoptosis of EBVtransformed LCLs.-
dc.languageeng-
dc.publisherMedcom Limited. The Journal's web site is located at http://www.hkjpaed.org/index.asp-
dc.relation.ispartofHong Kong Journal of Paediatrics (New series)-
dc.subjectPediatrics-
dc.titleCombination of HDAC and proteasome inhibitors up-regulates P16INK4A and P21WAF1 and induces apoptosis of EBV-Transformed lymphoblastoid cell lines-
dc.typeConference_Paper-
dc.identifier.emailHui, KF: kfhui@hku.hk-
dc.identifier.emailChiang, AKS: chiangak@hku.hk-
dc.identifier.authorityChiang, AKS=rp00403-
dc.identifier.hkuros243059-
dc.identifier.volume19-
dc.identifier.issue3-
dc.identifier.spage205-
dc.identifier.epage205-
dc.publisher.placeHong Kong-

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