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首页> 外文期刊>Life sciences >Vincristine-resistant human laryngeal carcinoma cells demonstrate increased Rous sarcoma virus promoter activity.
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Vincristine-resistant human laryngeal carcinoma cells demonstrate increased Rous sarcoma virus promoter activity.

机译：长春新碱耐药的人喉癌细胞显示出劳斯肉瘤病毒启动子活性增强。

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AIMS: Gene therapy is a candidate approach for treating cancer patients whose tumors have developed resistance to some drugs. Our study aims to examine possible alteration in Ad5RSVbetagal-mediated transgene expression in a vincristine-resistant cells (VK2) derived from the human laryngeal carcinoma cell line HEp2, and the underlying mechanism(s) thereof. MAIN METHODS: Adenovirus-mediated transgene expression in HEp2 and VK2 cells was measured by beta-gal staining. Semiquantitative PCR was used to evaluate attachment of adenovirus to the cell surface and adenovirus internalization into cells. After transfection of cells with plasmid DNA, promoter activity was measured by semiquantitative RT-PCR. KEY FINDINGS: We show here that VK2 cells exhibited increased Ad5RSVbetagal-mediated transgene expression, despite moderately decreased Ad5RSVbetagal attachment and internalization, as compared with HEp2 cells. The increased transgene expression was also observed with a virus (Ad5FbDelta639RSVbetagal) that does not use the coxsackie-adenovirus receptor (CAR), suggesting that increased transgene expression is independent of CAR. Upon transfection of VK2 cells with a plasmid expressing a reporter gene under the control of the RSV promoter or a plasmid containing the complete Ad5RSVbetagal genome, RSV promoter activity was 33- and 4.7-fold higher, respectively, than in HEp2 cells. SIGNIFICANCE: The increased Ad5RSVbetagal-mediated transgene expression in the VK2 cells is due to the increased RSV promoter activity in VK2 cells. Our results point out that (i) drug-resistance may be accompanied with an alteration in promoter activity; (ii) the proper choice of promoter could contribute to a decrease in the vector dose required to achieve a therapeutic effect during gene therapy.
机译：目的：基因治疗是治疗肿瘤对某些药物产生耐药性的癌症患者的候选方法。我们的研究旨在检查源自人喉癌细胞系HEp2的长春新碱抗性细胞（VK2）中Ad5RSVbetagal介导的转基因表达的可能变化及其潜在机制。主要方法：腺病毒介导的转基因在HEp2和VK2细胞中的表达通过beta-gal染色进行了测量。使用半定量PCR评估腺病毒对细胞表面的附着以及腺病毒内化进入细胞的能力。用质粒DNA转染细胞后，通过半定量RT-PCR测量启动子活性。主要发现：与HEp2细胞相比，尽管Ad5RSVbetagal附着和内在化程度有所降低，但我们在这里显示VK2细胞显示出Ad5RSVbetagal介导的转基因表达增加。在不使用柯萨奇腺病毒受体（CAR）的病毒（Ad5FbDelta639RSVbetagal）中也观察到转基因表达增加，这表明转基因表达增加与CAR无关。用表达报告基因的质粒在RSV启动子的控制下转染VK2细胞或含有完整Ad5RSVbetagal基因组的质粒转染VK2细胞时，RSV启动子活性分别比HEp2细胞高33倍和4.7倍。意义：VK2细胞中Ad5RSVbetagal介导的转基因表达增加是由于VK2细胞中RSV启动子活性增加。我们的结果指出：（i）耐药性可能伴随启动子活性的改变; （ii）适当选择启动子可有助于减少基因治疗期间达到治疗效果所需的载体剂量。

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