TCF4N剪接异构体在食管癌细胞中的表达研究

罗超; 何刚; 官兴颖; 唐敏; 刘双; 甘生敏; 李娟; 彭志平; 章波

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TCF4N剪接异构体在食管癌细胞中的表达研究

论著 | 更新时间：2026-01-09

- TCF4N剪接异构体在食管癌细胞中的表达研究
- Identification of T cell factor 4N isoform in esophageal cancer cell line EC109
- 陆军军医大学学报 2014年36卷第24期页码：2476-2480
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  中图分类号： R394-33;R394.2;R735.1
- 纸质出版：2014
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罗超,何刚,官兴颖,唐敏,刘双,甘生敏,李娟,彭志平,章波.TCF4N剪接异构体在食管癌细胞中的表达研究[J].陆军军医大学学报(原第三军医大学学报),2014,36(24):2476-2480.

　Luo Chao,He Gang,Guan Xingying,Tang Min,Liu Shuang,Gan Shengmin,Li Juan,Peng Zhiping,Zhang Bo.Identification of T cell factor 4N isoform in esophageal cancer cell line EC109[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(24):2476-2480.
罗超,何刚,官兴颖,唐敏,刘双,甘生敏,李娟,彭志平,章波.TCF4N剪接异构体在食管癌细胞中的表达研究[J].陆军军医大学学报(原第三军医大学学报),2014,36(24):2476-2480. DOI：

　Luo Chao,He Gang,Guan Xingying,Tang Min,Liu Shuang,Gan Shengmin,Li Juan,Peng Zhiping,Zhang Bo.Identification of T cell factor 4N isoform in esophageal cancer cell line EC109[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(24):2476-2480. DOI：

摘要

目的证实食管癌中TCF4N剪接异构体的存在，并初步探讨其功能。方法采用RT-PCR方法扩增，并PCR产物测序鉴定。克隆TCF4N剪接异构体并构建真核表达载体，将其转染EC109细胞高效表达，检测其对细胞生物学特性的影响。结果在癌细胞株中，TCF4N剪接异构体被证实存在。对比食管癌组织与癌旁组织发现TCF4N异构体在癌组织中表达显著降低(P0.05)。成功构建了TCF4N表达载体，在EC109细胞中获得高效表达。功能分析显示：增强TCF4N表达可抑制EC109细胞的增殖，影响细胞周期的分布，并抑制TCF4的转录活性。结论在人食管癌中具有抑制功能的TCF4N剪接异构体与食管癌的发生有一定关联。

Abstract

Objective To identify the existence and to explore the function of T cell factor 4N (TCF4N) splicing isoform in human esophageal cancer cell EC109. Methods RT-PCR technology was applied to amplify the specific exon of TCF4N and the product was further sequenced. The coding region of TCF4N was amplified and further ligated to the eukaryotic expression vector. The recombinant vector

which was verified by sequencing

was then transfected into the EC109 cells to detect its roles. Results The TCF4N splicing isoform existed in human esophageal cancer cell line

as well as esophageal tissues. Compared with that of the adjacent tissues

TCF4N was down-regulated in the esophageal cancer tissues. The TCF4N expression vector was successfully constructed

and effectively expressed in the EC109 cells. Functional analysis showed high level expression of TCF4N led to inhibition of cell growth

cell cycle redistribution and attenuation of TCF4 transcription activity. Conclusion The TCF4N splicing isoform is an authentic expressed isoform in human esophageal cancer cells

and is relative to tumorigenesis of esophageal cancer.

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