Expression of GABA and GABRP in gastric cancer SGC-7901 cells and its effect on cell migration ability

Shi Lianghui; Zhang Caiquan

您当前的位置：

首页 >

文章列表页 >

Expression of GABA and GABRP in gastric cancer SGC-7901 cells and its effect on cell migration ability

更新时间：2025-01-15

- Expression of GABA and GABRP in gastric cancer SGC-7901 cells and its effect on cell migration ability
- Journal of Army Medical University Vol. 33, Issue 20, Pages: 2132-2135(2011)
- 作者机构：
  
  1. 重庆医科大学附属第一医院胃肠外科
  2. 皖南医学院弋矶山医院普外科
- 作者简介：
- 基金信息：
- DOI：
  CLC： R394.2;R735.2;R730.23
- Published：2011，
  
  Published Online：30 October 2011，
- 稿件说明：
移动端阅览
SHI LIANGHUI, ZHANG CAIQUAN. Expression of GABA and GABRP in gastric cancer SGC-7901 cells and its effect on cell migration ability. [J]. Journal of army medical university, 2011, 33(20): 2132-2135.
DOI：

SHI LIANGHUI, ZHANG CAIQUAN. Expression of GABA and GABRP in gastric cancer SGC-7901 cells and its effect on cell migration ability. [J]. Journal of army medical university, 2011, 33(20): 2132-2135. DOI：

摘要

目的观察GABA、GAD65、GABRP在胃癌SGC-7901细胞中的表达及对细胞增殖、细胞周期分布的影响。方法 RT-PCR、IF及Western Blot检测胃癌细胞SGC-7901中GABA、GAD65 及GABRP mRNA及蛋白表达；1、10、100 μmol/L GABA，0.5、5、50 μmol/L Muscimol，0.5、5、50 μmol/L Bicucullin分别作用于胃癌细胞SGC-7901 48 h后，新型四唑氮盐（MTS）比色法检测细胞增殖情况，流式细胞仪检测细胞周期分布情况。结果 GAD65、GABRP mRNA及蛋白均表达于SGC-7901细胞中；GABA、GABRP及GAD65蛋白定位于SGC-7901细胞细胞膜和细胞质；与空白组比较，1 μmol/L GABA，5、50 μmol/L Muscimol作用SGC-7901细胞48 h后，细胞生长的增殖率上升，5、50 μmol/L Bicucullin作用SGC-7901细胞48 h后，细胞生长抑制率上升；1 μmol/L GABA可导致细胞G

数量的减少，G

/M期数量的增加；3个浓度的Muscimol可导致G

期数量的减少，5、50μmol/L Muscimol可导致细胞G

/M期数量增加；5、50 μmol/L Bicucullin可导致G

M期数量的减少（

0.05）。结论 GABA及其A受体在SGC-7901细胞中的表达可能促进细胞增殖，扰乱细胞周期进程，促使细胞分裂。

Abstract

Objective To investigate the expression of γ- aminobutyric acid (GABA)

it’s a receptor (GABA

R) and L-glutamate decarboxylase 65 (GAD65) in human gastric cancer SGC-7901 cells and their effects on cell proliferation and cell cycle proportion.

Methods RT-PCR

Western blotting and immunofluorescent staining were used to detect the expression of GABA

GAD65 and GABA

R in SGC-7901 cells. SGC-7901 cells were also cultured for 48 h with 1

10 or 100 μmol/L GABA

0.5

5 or 50 μmol/L Muscimol (GABA

R agonist)

and 0.5

5 or 50 μmol/L Bicucullin (GABA

R antagonist) respectively. MTS assay was used to examine cell proliferation. Flow cytometry was used to analyze cell cycle distribution. Results The mRNA and protein of GABA

GAD65 and GABRP were all expressed in SGC-7901 cells. GABA

GAD65 and GABRP protein level were predominantly localized in the cell cytoplasm of SGC-7901. Compared with blank group

the cells proliferation were obviously stimulated after 1 μmol/L GABA and 5 and 50 μmol/L Muscimol treatment

but significantly inhibited after 5 and 50 μmol/L Bicucullin treatment. Flow cytometry analysis showed that the percentage of cells in G

phase were decreased while the cells in G

/M phase was increased after 1 μmol/L GABA treatment. Different concentrations of Muscimol reduced G

phase cell percentage

but both of 5 and 50 μmol/L concentrations of Muscimol elevated G

/M phase cell percentage. Bicucullin at 5 and 50 μmol/L resulted in reduction of the percentage of G

/M phase cells (

0.05). Conclusion Higher expression of GABA and GABA

R in SGC-7901 cells may promote cell proliferation

interfere cell cycle proceeding

and accelerate cell division.

关键词

胃肿瘤细胞系，肿瘤γ-氨基丁酸细胞增殖细胞周期

Keywords

gastric cancercell line tumorγ-aminobutyric acidcell proliferationcell cycle

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Effect of Tmub1 on mitosis of regenerating hepatocytes in rats

Function of circular RNA hsa_circ_0000711 in hepatocellular carcinoma cell lines

Roles and mechanisms of long non-coding RNA EHHADH-AS1 in HBV+ hepatocellular carcinoma

Effect of siRNA mediated down-regulation of AnnexinⅡ on human breast cancer cell line MDA-MB-435S

p38MAPK signal pathway modulates proliferation, apoptosis and cell cycle of rat hepatic stellate cells stimulated by acetaldehyde

Related Author

Fu Hangwei

Chen Jian

Xu Jianhua

Li Guangyao

Chen Ping

LIN Xia

ZHU Yuanxin

FU Hangwei

Related Institution

Department of Hepatobiliary Surgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University

Department of Hepatobiliary Surgery, Institute of Surgery Research, Third Affiliated Hospital, Army Medical University (Third Military Medical University)

Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital & Chongqing Cancer Institute & Chongqing Cancer Hospital

Cancer Center, Institute of Surgery Research, Third Affiliated Hospital, Army Medical University (Third Military Medical University)

Center of Hepatobiliary Pancreatic Disease, Beijing Tsinghua Changgung Hospital

⁰