Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.

Several unique biological features of HIV-1 Vpr make it a potentially powerful agent for anti-cancer therapy. First, Vpr inhibits cell proliferation by induction of cell cycle G2 arrest. Second, it induces apoptosis through multiple mechanisms, which could be significant as it may be able to overcom...

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Autores principales:	Richard Y Zhao, Dong Liang, Ge Li, Christopher W Larrimore, Bernard L Mirkin
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/38e811006a4e42b6a91be8d019a5a468
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spelling	oai:doaj.org-article:38e811006a4e42b6a91be8d019a5a4682021-12-02T20:20:16ZAnti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.1932-620310.1371/journal.pone.0011466https://doaj.org/article/38e811006a4e42b6a91be8d019a5a4682010-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20628645/?tool=EBIhttps://doaj.org/toc/1932-6203Several unique biological features of HIV-1 Vpr make it a potentially powerful agent for anti-cancer therapy. First, Vpr inhibits cell proliferation by induction of cell cycle G2 arrest. Second, it induces apoptosis through multiple mechanisms, which could be significant as it may be able to overcome apoptotic resistance exhibited by many cancerous cells, and, finally, Vpr selectively kills fast growing cells in a p53-independent manner. To demonstrate the potential utility of Vpr as an anti-cancer agent, we carried out proof-of-concept studies in vitro and in vivo. Results of our preliminary studies demonstrated that Vpr induces cell cycle G2 arrest and apoptosis in a variety of cancer types. Moreover, the same Vpr effects could also be detected in some cancer cells that are resistant to anti-cancer drugs such as doxorubicin (DOX). To further illustrate the potential value of Vpr in tumor growth inhibition, we adopted a DOX-resistant neuroblastoma model by injecting SK-N-SH cells into C57BL/6N and C57BL/6J-scid/scid mice. We hypothesized that Vpr is able to block cell proliferation and induce apoptosis regardless of the drug resistance status of the tumors. Indeed, production of Vpr via adenoviral delivery to neuroblastoma cells caused G2 arrest and apoptosis in both drug naïve and DOX-resistant cells. In addition, pre-infection or intratumoral injection of vpr-expressing adenoviral particles into neuroblastoma tumors in SCID mice markedly inhibited tumor growth. Therefore, Vpr could possibly be used as a supplemental viral therapeutic agent for selective inhibition of tumor growth in anti-cancer therapy especially when other therapies stop working.Richard Y ZhaoDong LiangGe LiChristopher W LarrimoreBernard L MirkinPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 7, p e11466 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Richard Y Zhao Dong Liang Ge Li Christopher W Larrimore Bernard L Mirkin Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.
description	Several unique biological features of HIV-1 Vpr make it a potentially powerful agent for anti-cancer therapy. First, Vpr inhibits cell proliferation by induction of cell cycle G2 arrest. Second, it induces apoptosis through multiple mechanisms, which could be significant as it may be able to overcome apoptotic resistance exhibited by many cancerous cells, and, finally, Vpr selectively kills fast growing cells in a p53-independent manner. To demonstrate the potential utility of Vpr as an anti-cancer agent, we carried out proof-of-concept studies in vitro and in vivo. Results of our preliminary studies demonstrated that Vpr induces cell cycle G2 arrest and apoptosis in a variety of cancer types. Moreover, the same Vpr effects could also be detected in some cancer cells that are resistant to anti-cancer drugs such as doxorubicin (DOX). To further illustrate the potential value of Vpr in tumor growth inhibition, we adopted a DOX-resistant neuroblastoma model by injecting SK-N-SH cells into C57BL/6N and C57BL/6J-scid/scid mice. We hypothesized that Vpr is able to block cell proliferation and induce apoptosis regardless of the drug resistance status of the tumors. Indeed, production of Vpr via adenoviral delivery to neuroblastoma cells caused G2 arrest and apoptosis in both drug naïve and DOX-resistant cells. In addition, pre-infection or intratumoral injection of vpr-expressing adenoviral particles into neuroblastoma tumors in SCID mice markedly inhibited tumor growth. Therefore, Vpr could possibly be used as a supplemental viral therapeutic agent for selective inhibition of tumor growth in anti-cancer therapy especially when other therapies stop working.
format	article
author	Richard Y Zhao Dong Liang Ge Li Christopher W Larrimore Bernard L Mirkin
author_facet	Richard Y Zhao Dong Liang Ge Li Christopher W Larrimore Bernard L Mirkin
author_sort	Richard Y Zhao
title	Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.
title_short	Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.
title_full	Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.
title_fullStr	Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.
title_full_unstemmed	Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.
title_sort	anti-cancer effect of hiv-1 viral protein r on doxorubicin resistant neuroblastoma.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/38e811006a4e42b6a91be8d019a5a468
work_keys_str_mv	AT richardyzhao anticancereffectofhiv1viralproteinrondoxorubicinresistantneuroblastoma AT dongliang anticancereffectofhiv1viralproteinrondoxorubicinresistantneuroblastoma AT geli anticancereffectofhiv1viralproteinrondoxorubicinresistantneuroblastoma AT christopherwlarrimore anticancereffectofhiv1viralproteinrondoxorubicinresistantneuroblastoma AT bernardlmirkin anticancereffectofhiv1viralproteinrondoxorubicinresistantneuroblastoma
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Anti-cancer effect of HIV-1 viral protein R on doxorubicin resistant neuroblastoma.

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