Effect of transcription elongation factor A (S Ⅱ) like 7 on proliferation, migration, invasion and apoptosis of colorectal cancer cells

Li CHENG; Zheng JIANG

doi:10.16016/j.1000-5404.201709109

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Effect of transcription elongation factor A (S Ⅱ) like 7 on proliferation, migration, invasion and apoptosis of colorectal cancer cells

Basic Medicine | 更新时间：2026-01-09

- Effect of transcription elongation factor A (S Ⅱ) like 7 on proliferation, migration, invasion and apoptosis of colorectal cancer cells
- Journal of Third Military Medical University Vol. 40, Issue 3, Pages: 230-236(2018)
- 作者机构：
  
  400016 重庆，重庆医科大学附属第一医院消化内科
- 作者简介：
- 基金信息：
- DOI：10.16016/j.1000-5404.201709109
  CLC： R394.3;R730.23;R735.35
- Received：14 September 2017，
  
  Revised：2017-10-17，
  
  Published：15 February 2018
- 稿件说明：
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Li CHENG, Zheng JIANG. Effect of transcription elongation factor A (S Ⅱ) like 7 on proliferation, migration, invasion and apoptosis of colorectal cancer cells[J]. Journal of Third Military Medical University, 2018, 40(3): 230-236.
DOI：

Li CHENG, Zheng JIANG. Effect of transcription elongation factor A (S Ⅱ) like 7 on proliferation, migration, invasion and apoptosis of colorectal cancer cells[J]. Journal of Third Military Medical University, 2018, 40(3): 230-236. DOI： 10.16016/j.1000-5404.201709109.

摘要

目的

探讨TCEAL7[transcription elongation factor A(SⅡ)like 7]对结直肠癌细胞生物学功能的影响及可能的作用机制。

方法

应用RT-PCTCEAL7在结直肠癌细胞Caco2、HT29、HCT116、SW480以及正常结直肠组织中的表达水平，筛选出低表达的细胞

将重组质粒pEZ-M98-TCEAL7及空质粒pEZ-M98通过脂质体Lipofectamine 2000转染Caco2细胞，应用RT-PCR及Western blot分别检测TCEAL7的mRNA以及蛋白表达水平；CCK-8和克隆形成实验检测细胞增殖活力，Transwell检测细胞迁移及侵袭能力，流式细胞术检测细胞凋亡；Western blot检测NF-κB及其下游靶基因蛋白表达的变化情况。

结果

TCEAL7在结直肠癌细胞Caco2、HT29、HCT116、SW480中的mRNA表达量分别为(0.19±0.02)、(0.25±0.03)、(0.30±0.03)、(0.28±0.04)，与正常结直肠组织(1.03±0.03)、(1.06±0.07)相比明显下降(

0.01)。Caco2细胞转染组TCEAL7 mRNA和蛋白表达量分别为(1.08±0.13)、(1.01±0.15)，均明显高于对照组[(0.43±0.20)、(0.53±0.10)

0.01

]

。与对照组相比，转染组Caco2细胞的增殖、迁移及侵袭能力明显降低(

0.01)，细胞凋亡增加(

0.01)，NF-κB及其下游靶基因蛋白表达改变(

0.01)。

结论

TCEAL7在结直肠癌细胞中为低表达，过表达TCEAL7能抑制Caco2细胞增殖、迁移及侵袭，促进细胞凋亡，可能与NF-κB信号通路有关。

Abstract

Objective

To determine the effect of transcription elongation factor A (SⅡ) like 7 (TCEAL7) on the biological functions in colorectal cancer cells and investigate the underlying mechanism.

Methods

The expression of TCEAL7 in colorectal cancer cell lines Caco2

HT29

HCT116 and SW480

and normal colorectal tissues was investigated by RT-PCR in order to screen the colorectal cancer cells with low expression level of TCEAL7. Then

the recombinant plasmid pEZ-M98-TCEAL7 and blank vector pEZ-M98 were transfected into Caco2 cells by Lipofectamine 2000

the mRNA and protein levels of TCEAL7 were tested by RT-PCR and Western blotting respectively. CCK-8 assay and colony formation assay were applied to analyze the cell proliferation. Transwell chamber test was performed to measure the migration and invasion ability of the cells. Flow cytometry was conducted to analyze the cell apoptosis. Western blotting was employed to detect the protein expression changes of NF-κB and the downstream targets.

Results

The mRNA level of TCEAL7 in the colorectal cancer Caco2

HT29

HCT116 and SW480 cells was 0.19±0

.02

0.25±0.03

0.30±0.03

and 0.28±0.04

respectively

significantly lower than those of normal colorectal tissues (1.03±0.03 and 1.06±0.07

0.01). The mRNA and protein levels of TCEAL7 in the pEZ-M98-TCEAL7 transfected group were significantly higher than those in the pEZ-M98 control group (1.08±0.13

0.43±0.20

1.01±0.15

0.53±0.10

0.01). When compared to the control group

the transfected group had markedly inhibited cells proliferation

decreased abilities of migration and invasion (

0.01)

promoted cell apoptosis (

0.01)

and altered the protein expression of NF-κB and the downstream targets (

0.01).

Conclusion

TCEAL7 is lowly expressed in colorectal cancer cell lines. Over-expression of TCEAL7 evidently inhibits the proliferation

migration and invasion

and induces apoptosis in colorectal cancer Caco2 cells

which may be through NF-κB signaling pathway.

关键词

Keywords

references

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