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首页> 外文期刊>Cell cycle >Hypoxia enhances the replication of oncolytic herpes simplex virus in p53- breast cancer cells.
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Hypoxia enhances the replication of oncolytic herpes simplex virus in p53- breast cancer cells.

机译：缺氧增强了溶瘤性单纯疱疹病毒在p53-乳腺癌细胞中的复制。

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摘要

Hypoxic cancer cells are refractory to conventional chemotherapy. Herpes simplex virus type-1 (HSV-1)-derived oncolytic viruses are safe for therapy since they lack the neurovirulence gene ICP34.5. Cancer cells containing high MEK activity are permissive to the HSV-1-derived oncolytic virus, R3616. Considering that hypoxia increases MEK activity, we determined whether hypoxic MDA-MB-231 and MCF-7 cells were more permissive to R3616, compared to normoxic cells. We observed nine-fold higher (3.5 x 10e6 pfu/4 x 10e5 pfu/ml) titers in MDA-MB-231 hypoxic cells compared to normoxic; however, hypoxic MCF-7 cells did not yield higher R3616 titers. Markers for early and late viral infection were consistent with this result: (1) virus-induced chaperone-enriched (VICE) domains were observed in MDA-MB-231 cells, and (2) the HSV-1 glycoprotein C (gC), a protein produced late in infection, accumulated in hypoxic MDA-MB-231 cells. Thus, oncolytic R3616 virus may target hypoxic p53(-) breast cancer cells.
机译：缺氧癌细胞对常规化疗是难治的。单纯疱疹病毒1型（HSV-1）衍生的溶瘤病毒由于缺乏神经毒力基因ICP34.5，因此可以安全治疗。含有高MEK活性的癌细胞被HSV-1衍生的溶瘤病毒R3616允许。考虑到缺氧会增加MEK活性，我们确定了缺氧MDA-MB-231和MCF-7细胞是否比常氧细胞更适合R3616。我们观察到MDA-MB-231低氧细胞的滴度比常氧高9倍（3.5 x 10e6 pfu / 4 x 10e5 pfu / ml）。然而，低氧MCF-7细胞不能产生更高的R3616效价。早期和晚期病毒感染的标记与该结果一致：（1）在MDA-MB-231细胞中观察到病毒诱导的伴侣富集（VICE）域，（2）HSV-1糖蛋白C（gC）感染后期产生的一种蛋白质，积累在低氧的MDA-MB-231细胞中。因此，溶瘤性R3616病毒可能靶向缺氧的p53（-）乳腺癌细胞。

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