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血管内皮生长因子-C对鼻咽癌CNE-2细胞小鼠移植瘤的辐射敏感性的影响
作者姓名:吴锡芳  汪勇  彭丽莎  罗洁  王枫
作者单位:1.昆明医科大学第三附属医院头颈外科,云南 昆明 650118
基金项目:云南省科技厅-昆明医科大学应用基础研究联合专项基金资助项目(2019FE001)
摘    要:  目的  探讨干扰VEGF-C表达可以增加鼻咽癌CNE-2细胞小鼠移植瘤辐射敏感性作用以及相关信号途径。  方法  鼻咽癌CNE-2小鼠移植瘤随机分为:瘤体组;siRNA-NC组;siRNA-VEGF-C组;照射组;siRNA-NC+照射组;siRNA-VEGF-C+照射组。观察肿瘤生长情况;采用免疫组化检测VEGF-C、ATM、P65蛋白的表达变化。  结果  干扰VEGF-C表达鼻咽癌CNE-2细胞小鼠移植瘤,在照射后明显肿瘤生长明显变慢。免疫组化检测结果显示:干扰VEGF-C小鼠移植瘤后,VEGF-C、ATM明显减少(P < 0.05),P65增加(P < 0.05);联合照射后,VEGF-C、ATM明显减少(P < 0.05)。  结论  在鼻咽癌CNE-2细胞小鼠移植瘤中,干扰VEGF-C基因通过激活NF-kB信号通路影响下游ATM,进而增加放疗敏感性。

关 键 词:鼻咽癌    血管内皮生长因子-C    辐射敏感性    实验动物
收稿时间:2021-12-06

Effect of VEGF-C on Radiation Sensitivity of Nasopharyngeal Carcinoma CNE-2 Cell Transplanted Mice
Institution:1.Dept. of Head and Neck Surgery,The 3rd Affiliated Hospital of Kunming Medical University,Kunming Yunnan 6501182.Dept. of Radiotherapy,The 1st Affiliated Hospital of Kunming Medical University,Kunming Yunnan 650032,China
Abstract:  Objective   To investigate the effect of interfering with the expression of VEGF-C on the radiosensitivity of the nasopharyngeal carcinoma CNE-2 cell transplanted tumor and related signaling pathways.   Methods  The mice with transplanted tumors of nasopharyngeal carcinoma CNE-2 were randomly divided into tumor body group, siRNA-NC group, siRNA-VEGF-C group; irradiation group; siRNA-NC+ irradiation group; siRNA-VEGF-C+irradiation group. Tumor growth was observed, and the protein expression of VEGF-C, ATM and P65 were detected by immunohistochemistry.   Results  Interference of VEGF-C expression in nasopharyngeal carcinoma CNE-2 cell transplanted tumors showed significantly slower tumor growth after irradiation. Immunohistochemical test results showed that after tumor transplantation of mice interfered with VEGF-C, VEGF-C and ATM were significantly decreased (P < 0.05), while P65 was increased (P < 0.05). After combined irradiation, VEGF-C and ATM were significantly decreased (P < 0.05).  Conclusion  In mouse nasopharyngeal carcinoma CNE-2 cell transplantation tumors, interfering with VEGF-C gene affects downstream ATM by activating NF-kB signaling pathway, thereby increasing the sensitivity of radiotherapy.
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