过表达CBX7调控PTEN/Akt信号通路干预上皮-间充质转化抑制胃癌细胞迁移、侵袭

谭斌; 刘剑波; 李芳芳; 彭艳; 钟月圆; 邓晖; 王秀丽

doi:10.11659/jjssx.04E022092

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过表达CBX7调控PTEN/Akt信号通路干预上皮-间充质转化抑制胃癌细胞迁移、侵袭

基础研究 | 更新时间：2023-05-26

- 过表达CBX7调控PTEN/Akt信号通路干预上皮-间充质转化抑制胃癌细胞迁移、侵袭
- Overexpression of CBX7 inhibits the migration and invasion of gastric cancer cells by regulating PTEN/Akt signaling pathway to interfere epithelial-mesenchymal transition
- 局解手术学杂志 2023年32卷第5期页码：394-399
- 作者机构：
  
  郴州市第一人民医院中心医院消化内科，湖南郴州 423000
- 作者简介：
  
  王秀丽，E-mail：814981848@qq.com
- 基金信息：
- DOI：10.11659/jjssx.04E022092
  中图分类号： R735.2
- 纸质出版日期：2023-05-25，
  
  收稿日期：2022-04-22，
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谭斌,刘剑波,李芳芳等.过表达CBX7调控PTEN/Akt信号通路干预上皮-间充质转化抑制胃癌细胞迁移、侵袭[J].局解手术学杂志,2023,32(05):394-399.

TAN Bin,LIU Jian-bo,LI Fang-fang,et al.Overexpression of CBX7 inhibits the migration and invasion of gastric cancer cells by regulating PTEN/Akt signaling pathway to interfere epithelial-mesenchymal transition[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2023,32(05):394-399.
谭斌,刘剑波,李芳芳等.过表达CBX7调控PTEN/Akt信号通路干预上皮-间充质转化抑制胃癌细胞迁移、侵袭[J].局解手术学杂志,2023,32(05):394-399. DOI： 10.11659/jjssx.04E022092.

TAN Bin,LIU Jian-bo,LI Fang-fang,et al.Overexpression of CBX7 inhibits the migration and invasion of gastric cancer cells by regulating PTEN/Akt signaling pathway to interfere epithelial-mesenchymal transition[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2023,32(05):394-399. DOI： 10.11659/jjssx.04E022092.

摘要

目的

探讨染色体盒蛋白同源物7（CBX7）对胃癌细胞上皮-间充质转化（EMT）、迁移、侵袭的影响及相关作用机制。

方法

将CBX7过表达质粒和阴性对照质粒、CBX7 siRNA和阴性对照siRNA转染至体外培养的人胃癌细胞SGC7901。采用qRT-PCR和Western blot法检测细胞中CBX7的mRNA和蛋白表达，CCK-8法检测细胞增殖情况，细胞划痕实验检测细胞迁移情况，Transwell小室检测细胞侵袭情况，Western blot法检测细胞中EMT相关蛋白和磷酸酶张力蛋白同源物基因（PTEN）/蛋白激酶B（Akt）信号通路相关蛋白表达。

结果

与pcDNA-NC组比较，pcDNA-CBX7组SGC7901细胞存活率、迁移率及侵袭数均显著下降/减少，细胞中E-钙黏蛋白（E-cadherin）、PTEN蛋白表达量均显著升高，N-钙黏蛋白（N-cadherin）和波形蛋白（Vimentin）蛋白表达量、p-Akt/Akt均显著下降，差异有统计学意义（

0.05）。与si-NC组比较，si-CBX7组SGC7901细胞存活率、迁移率及侵袭数均显著升高/增加，细胞中E-cadherin、PTEN蛋白表达量均显著下降，N-cadherin、Vimentin蛋白表达量和p-Akt/Akt均显著升高，差异有统计学意义（

0.05）。

结论

过表达CBX7可通过抑制EMT进程抑制胃癌细胞迁移、侵袭，其作用机制可能与调控PTEN/Akt信号通路有关。

Abstract

Objective

To investigate the effects and related mechanisms of chromosome box protein homologue 7 (CBX7) on epithelial-mesenchymal transition (EMT)

migration and invasion in gastric cancer cells.

Methods

The CBX7 overexpression plasmid and negative control plasmid

CBX7 siRNA and negative control siRNA were transfected into human gastric cancer cells SGC7901 cultured in vitro.The mRNA and protein expression of CBX7 in cells were detected by qRT-PCR and Western blot

the cell proliferation was detected by CCK-8 method

the cell migration was detected by scratch wound healing assay

the cell invasion was detected by Transwell assay

the expression of cell EMT related proteins and phosphatase tension protein homologue gene (PTEN)/protein kinase B (Akt) signaling pathway related proteins were detected by Western blot.

Results

Compared with the pcDNA-NC group

the survival rate

migration rate and invasion number of SGC7901 cells in the pcDNA-CBX7 group were significantly decreased

the protein expression of E-cadherin and PTEN in cells were significantly increased

and the protein expression of N-cadherin

Vimentin and the ratio of p-Akt/Akt were significantly decreased

with statistically significant differences (

0.05).Compared with the si-NC group

the survival rate

migration rate and invasion number of SGC7901 cells in the si-CBX7 group were significantly increased

the protein expression of E-cadherin and PTEN in cells were significantly decreased

and the protein expression of N-cadherin

Vimentin and the ratio of p-Akt/Akt were significantly increased

with statistically significant differences (

0.05).

Conclusion

Overexpression of CBX7 can inhibit the migration and invasion of gastric cancer cells by inhibiting the EMT process

and its mechanism may be related to the regulation of PTEN/Akt signaling pathway.

关键词

染色体盒蛋白同源物7胃癌上皮-间充质转化迁移侵袭PTEN/Akt信号通路

Keywords

chromosome box protein homologue 7gastric cancerepithelial-mesenchymal transitionmigrationinvasionPTEN/Akt signaling pathway

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