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NF-κB p65小干扰RNA对裸鼠人喉癌移植瘤模型的抑制作用

[Inhibitory effect of NF-kappaB p65siRNA on human laryngeal carcinoma xenograft model in nude mice].

作者信息

Jin Hongjun, Lou Weihua, Sang Jianzhong

机构信息

Department of Otorhinolaryngology-Head and Neck Surgery, the First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, China.

出版信息

Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2013 Aug;27(15):836-8.

Abstract

OBJECTIVE

To investigate the inhibitory effect of NF-kappaB p65siRNA on human laryngeal carcinoma xenograft model in nude mice.

METHOD

Human laryngeal carcinoma cell line Hep-2 was seeded in the subcutaneous layer of 15 nude mice to build laryngeal carcinoma xenograft model. Then they were randomly divided into three groups. NF-kappaB p65siRNA was given in siRNA group and FAM-Control siRNA was given in negative control group while phosphoric-buffered saline (PBS) was used in normal control group for 3 weeks. Tumor size and body weight of the mice were measured. TUNEL method and immunohistochemical S-P method were used for detecting the expression of NF-kappaB p65 and Bcl-xL protein.

RESULT

The volume of tumors in siRNA group was reduced and the average weight of tumors in siRNA group was lower than the other two groups (P < 0.05). In siRNA group, the expression of NF-kappaB p65 and Bcl-xL protein was down-regulated and the apoptotic rate was increased obviously as compared with the negative control group and the normal control group.

CONCLUSION

NF-kappaB p65siRNA can significantly inhibit the expression of NF-kappaB p65 and the growth of human laryngeal carcinoma xenograft in nude mice. Its mechanism may be related to inducing the apoptosis in tumor cells by down-regulating the expression of Bcl-xL protein.

摘要

目的

探讨NF-κB p65小干扰RNA(siRNA)对人喉癌裸鼠移植瘤模型的抑制作用。

方法

将人喉癌细胞系Hep-2接种于15只裸鼠皮下建立喉癌移植瘤模型。然后将其随机分为三组。siRNA组给予NF-κB p65 siRNA,阴性对照组给予FAM-对照siRNA,正常对照组给予磷酸缓冲液(PBS),持续3周。测量小鼠的肿瘤大小和体重。采用TUNEL法和免疫组织化学S-P法检测NF-κB p65和Bcl-xL蛋白的表达。

结果

siRNA组肿瘤体积减小,siRNA组肿瘤平均重量低于其他两组(P<0.05)。与阴性对照组和正常对照组相比,siRNA组中NF-κB p65和Bcl-xL蛋白的表达下调,凋亡率明显增加。

结论

NF-κB p65 siRNA可显著抑制NF-κB p65的表达及人喉癌裸鼠移植瘤的生长。其机制可能与下调Bcl-xL蛋白表达诱导肿瘤细胞凋亡有关。

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