2006
DOI: 10.1038/sj.cgt.7700957
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Enhancement of antitumor activity of herpes simplex virus γ134.5-deficient mutant for oral squamous cell carcinoma cells by hexamethylene bisacetamide

Abstract: Current oncolytic viruses exert only limited antitumor activity on their own. There is a need to increase their oncolytic capability. We evaluated the effect of a differentiating reagent, hexamethylene bisacetamide (HMBA), on the antitumor activity of a g 1 34.5-deficient herpes simplex virus type 1 (HSV-1) R849 for human oral squamous cell carcinoma (SCC) cells. Hexamethylene bisacetamide increased the viral yield, especially at a low input multiplicity of infection (MOI), and the transcription of immediate e… Show more

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Cited by 13 publications
(15 citation statements)
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References 36 publications
(48 reference statements)
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“…32 Previously, we indicated that g 1 34.5-deficient HSV-1 could replicate in oral SCC cells. 9 In this study, we examined the effect of infection by a g 1 34.5-deficient HSV-1 mutant on the distribution of p65 in oral SCC cells and found that NF-kB components were increased in the nucleus after infection. The increase in NFkB was confirmed by immunofluorescent staining and a similar translocation of NF-kB was observed in other oral SCC cell lines, such as Ca9-22 and HSC cells (data not shown).…”
Section: Discussionmentioning
confidence: 99%
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“…32 Previously, we indicated that g 1 34.5-deficient HSV-1 could replicate in oral SCC cells. 9 In this study, we examined the effect of infection by a g 1 34.5-deficient HSV-1 mutant on the distribution of p65 in oral SCC cells and found that NF-kB components were increased in the nucleus after infection. The increase in NFkB was confirmed by immunofluorescent staining and a similar translocation of NF-kB was observed in other oral SCC cell lines, such as Ca9-22 and HSC cells (data not shown).…”
Section: Discussionmentioning
confidence: 99%
“…Studies exploring chemotherapy-oncolytic virus combinations or viruses encoding therapeutic transgenes have demonstrated that synergistic tumor killing can either be replication-dependent, with enhanced replication resulting in enhanced potency, [4][5][6]9 or replication-independent, with enhanced potency being caused by mechanisms other than enhanced viral replication. 7,8 We found that TSA had a suppressive effect on the growth of oral SCC cells at 0.3 mM, but its effect was insufficient at 0.1 mM.…”
Section: Discussionmentioning
confidence: 99%
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“…In an animal study, the growth of nude mouse tumors was markedly suppressed by R849 in combination with HMBA and the survival of co-treated animals was significantly longer than that of animals treated with R849 only. HMBA enhances the antitumor activity of an inoculated virus through the expression of immediate early genes without increasing its toxicity [64]. It may be useful as an enhancing agent for oncolytic therapy with HSV-1 in cancer patients.…”
Section: New Combination Therapymentioning
confidence: 99%