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Inhibition of nuclear factor-kappaB activity by small interfering RNA in esophageal squamous cell carcinoma cell lines

wanyair 添加于 2011-11-9 16:15 | 2182 次阅读 | 0 个评论

作者
Hatata T, Higaki K, Nanba E, Tatebe S, Ikeguchi M
摘要
Chemotherapy with 5-fluorouracil (5-FU) is commonly used in combination therapy for esophageal squamous cell carcinoma (ESCC), but its efficacy is limited in certain patients. Recent studies suggest that constitutive activation of nuclear factor-kappaB (NF-kappaB) has a critical role in tumorigenesis and is associated with poor prognosis and resistance to chemoradiation therapy in many types of human cancers. In the present study, we evaluated the effect of small interfering RNA targeting NF-kappaB (NF-kappaB siRNA) combined with 5-FU on the proliferation of two cell lines of cultured ESSCs. Immunofluorescence and immunoblot analyses revealed that the NF-kappaB protein was localized mostly in the cytoplasm of ESCCs. When cultured ESCCs were exposed to tumor necrosis factor-alpha, NF-kappaB was transferred to the nucleus and activated. ESCCs with activated NF-kappaB had poor sensitivity to 5-FU. When cells were transfected with NF-kappaB siRNA, the levels of NF-kappaB protein were significantly decreased in the cytoplasm and the nucleus. Transcriptional activity of NF-kappaB was significantly suppressed in cells treated with 5-FU and NF-kappaB siRNA compared to cells treated with 5-FU alone. 5-FU consistently suppressed proliferation of ESCCs in a dose-dependent manner, and this effect was significantly enhanced when combined with NF-kappaB siRNA. These results suggest that combination therapy of 5-FU with NF-kappaB siRNA may provide a new therapeutic option for ESCC.
详细资料
- 文献种类:期刊
- 期刊名称: Oncology Reports
- 期刊缩写: Oncol Rep
- 期卷页: 2011年第26卷第3期 659-664页
- 地址: Division of Surgical Oncology, Department of Surgery, Faculty of Medicine, Research Center for Bioscience and Technology, Tottori University, Yonago, Japan
- ISBN: 1021-335X
- 备注:PMID:21617867
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与5 - 氟脲嘧啶（5 - FU）化疗结合治疗食管鳞状细胞癌（ESCC），常用，但其疗效在某些患者有限。最近的研究表明，核因子-κB（NF -κB的）在肿瘤形成中的一个关键作用，并与预后差，在许多类型的人类癌症抗放化疗治疗相关的构激活。在本研究中，我们评估针对的NF -κB（NF -κB的干扰）与5 - FU的两个细胞株培养ESSCs的增殖相结合的小分子干扰核糖核酸的效果。免疫荧光和免疫印迹分析显示，NF -κB蛋白主要定位于细胞质的ESCCs。培养ESCCs时暴露于肿瘤坏死因子-α，NF -κB的被转移到细胞核并激活。与NF -κB的激活ESCCs对5 - FU的敏感性差。当细胞NF -κB的siRNA的转染，细胞质和细胞核中NF -κB蛋白的水平显着下降。与5 - FU和NF -κB的siRNA处理的细胞相比，细胞与5 - FU单治疗显着抑制NF -κB的转录活性。5 - FU一直压制在剂量依赖的方式ESCCs扩散，并与NF -κB的siRNA的结合时，这种效应显着增强。这些结果表明，与NF -κB的siRNA的结合5 - FU的治疗食管鳞癌的治疗提供了新的选项。

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