An oncolytic adenovirus enhances antiangiogenic and antitumoral effects of a replication-deficient adenovirus encoding endostatin by rescuing its selective replication in nasopharyngeal carcinoma cells

Liu, Ran Yi; Zhou, Ling; Zhang, Yan Ling; Huang, Bi; Ke, Miao La; Chen, Jiemin; Li, Li xia; Fu, Xiang; Wu, Jiang; Huang, Wenlin

doi:10.1016/j.bbrc.2013.11.047

Cited by 11 publications

(7 citation statements)

References 17 publications

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“… 49 Ad-uPAR-MMP-9 is a replication-deficient adenovirus expressing antisense urokinase receptor (uPAR) and antisense Matrix metallopeptidase (MMP)-9, and therefore inhibits the expression of these important angiogenic targets in tumor tissues. 50 Other adenoviral vectors exert antiangiogenic effects in vitro and in vivo by expressing anti-angiogenic molecules, including endostatin, 51 angiostatin, 52 or an endostatin/angiostatin fusion. 53 Armed adenoviruses can reach the tumor vasculature via circulating endothelial progenitor (CEP) cells.…”

Section: Oncolytic Viral Platforms Associated With Vascular Targetingmentioning

confidence: 99%

Targeting tumor vasculature through oncolytic virotherapy: recent advances

Bejarano¹,

Merchan²

2015

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The oncolytic virotherapy field has made significant advances in the last decade, with a rapidly increasing number of early- and late-stage clinical trials, some of them showing safety and promising therapeutic efficacy. Targeting tumor vasculature by oncolytic viruses (OVs) is an attractive strategy that offers several advantages over nontargeted viruses, including improved tumor viral entry, direct antivascular effects, and enhanced antitumor efficacy. Current understanding of the biological mechanisms of tumor neovascularization, novel vascular targets, and mechanisms of resistance has allowed the development of oncolytic viral vectors designed to target tumor neovessels. While some OVs (such as vaccinia and vesicular stomatitis virus) can intrinsically target tumor vasculature and induce vascular disruption, the majority of reported vascular-targeted viruses are the result of genetic manipulation of their viral genomes. Such strategies include transcriptional or transductional endothelial targeting, “armed” viruses able to downregulate angiogenic factors, or to express antiangiogenic molecules. The above strategies have shown preclinical safety and improved antitumor efficacy, either alone, or in combination with standard or targeted agents. This review focuses on the recent efforts toward the development of vascular-targeted OVs for cancer treatment and provides a translational/clinical perspective into the future development of new generation biological agents for human cancers.

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Section: Oncolytic Viral Platforms Associated With Vascular Targetingmentioning

confidence: 99%

Targeting tumor vasculature through oncolytic virotherapy: recent advances

Bejarano¹,

Merchan²

2015

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“…Strategies targeting tumor vasculature have also involved oncolytic viruses [ 6 ]. Genetically-modified adenoviruses showing oncolytic and antiangiogenic properties have been combined to synergistically increase antitumor effect [ 7 ]. Entry of some oncolytic virus is mediated by specific or over-expressed receptors on the tumor cell surface [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Experimental Adaptation of Rotaviruses to Tumor Cell Lines

Guerrero

Silva

et al. 2016

PLoS ONE

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A number of viruses show a naturally extended tropism for tumor cells whereas other viruses have been genetically modified or adapted to infect tumor cells. Oncolytic viruses have become a promising tool for treating some cancers by inducing cell lysis or immune response to tumor cells. In the present work, rotavirus strains TRF-41 (G5) (porcine), RRV (G3) (simian), UK (G6-P5) (bovine), Ym (G11-P9) (porcine), ECwt (murine), Wa (G1-P8), Wi61 (G9) and M69 (G8) (human), and five wild-type human rotavirus isolates were passaged multiple times in different human tumor cell lines and then combined in five different ways before additional multiple passages in tumor cell lines. Cell death caused by the tumor cell-adapted isolates was characterized using Hoechst, propidium iodide, 7-AAD, Annexin V, TUNEL, and anti-poly-(ADP ribose) polymerase (PARP) and -phospho-histone H2A.X antibodies. Multiple passages of the combined rotaviruses in tumor cell lines led to a successful infection of these cells, suggesting a gain-of-function by the acquisition of greater infectious capacity as compared with that of the parental rotaviruses. The electropherotype profiles suggest that unique tumor cell-adapted isolates were derived from reassortment of parental rotaviruses. Infection produced by such rotavirus isolates induced chromatin modifications compatible with apoptotic cell death.

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“…In addition, the combination of H101 (an E1B-deleted adenovirus) and Ad-Endo significantly inhibited CNE-2 xenografts growth through increased endostatin expression and Ad replication. 15 Similar results were obtained using the E1B-55 K–attenuated adenovirus, dl 1520 in neural progenitor cells (NPCs) and xenografts in nude mice. Importantly, the antitumor activity of dl 1520 was augmented by the addition of cisplatin both in vitro and in vivo, showing that dl 1520 and cisplatin have a synergistic anti-NPC effect through oncolysis and the induction of apoptosis.…”

Section: Oncolytic Virotherapymentioning

confidence: 55%

Oncolytic virotherapy for head and neck cancer: current research and future developments

Malhotra

Sendilnathan

Old

et al. 2015

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Head and neck cancer (HNC) is the sixth most common malignancy worldwide. Despite recent advancements in surgical, chemotherapy, and radiation treatments, HNC remains a highly morbid and fatal disease. Unlike many other cancers, local control rather than systemic control is important for HNC survival. Therefore, novel local therapy in addition to systemic therapy is urgently needed. Oncolytic virotherapy holds promise in this regard as viruses can be injected intratumorally as well as intravenously with excellent safety profiles. This review will discuss the recent advancements in oncolytic virotherapy, highlighting some of the most promising candidates and modifications to date.

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An oncolytic adenovirus enhances antiangiogenic and antitumoral effects of a replication-deficient adenovirus encoding endostatin by rescuing its selective replication in nasopharyngeal carcinoma cells

Cited by 11 publications

References 17 publications

Targeting tumor vasculature through oncolytic virotherapy: recent advances

Targeting tumor vasculature through oncolytic virotherapy: recent advances

Experimental Adaptation of Rotaviruses to Tumor Cell Lines

Oncolytic virotherapy for head and neck cancer: current research and future developments

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