解剖学报 ›› 2022, Vol. 53 ›› Issue (3): 317-322.doi: 10.16098/j.issn.0529-1356.2022.03.007

• 肿瘤生物学 • 上一篇    下一篇

乙酰辅酶A羧化酶1对胶质瘤细胞系U87细胞增殖、迁移和侵袭的影响

王阳1 赵宝生2 李超红1,2 刘玉珍1,2*
  

  1. 1.新乡医学院第一附属医院生命科学研究中心,河南 卫辉453100; 2.新乡医学院第一附属医院胸外科,河南 卫辉 453100
  • 收稿日期:2020-08-02 修回日期:2020-11-17 出版日期:2022-06-06 发布日期:2019-06-06
  • 通讯作者: 刘玉珍 E-mail:yuzhenliu@xxmu.edu.com
  • 基金资助:
    新乡医学院第一附属医院博士基金;河南省科技厅科技攻关计划项目

Effects of acetyl-CoA carboxylase 1 on proliferation, migration and invasion of glioma cell line U87

WANG  Yang1  ZHAO  Bao-sheng2  LI  Chao-hong1,2  LIU  Yu-zhen1,2*   

  1. 1.Life Science Research Center, the First Affiliated Hospital of Xinxiang Medical University, He’nan Weihui 453100, China; 2.Department of Thoracic Surgery, the First Affiliated Hospital of Xinxiang Medical University, He’nan Weihui 453100, China
  • Received:2020-08-02 Revised:2020-11-17 Online:2022-06-06 Published:2019-06-06
  • Contact: LIU Yu-zhen E-mail:yuzhenliu@xxmu.edu.com

摘要:

目的 探讨乙酰辅酶A羧化酶1(ACC1)对人胶质瘤细胞系U87细胞增殖、迁移及侵袭的作用。  方法  Western blotting检测人胶质瘤细胞系U87、U251及U373中ACC1的表达;构建ACC1过表达质粒载体,将过表达ACC1质粒载体瞬时转染至U87细胞中;Western blotting检测转染后U87细胞中ACC1表达情况;MTT实验检测过表达ACC1对U87细胞增殖的影响;Transwell迁移和侵袭实验分别检测过表达ACC1对U87细胞迁移和侵袭的影响;划痕实验检测过表达ACC1对U87细胞划痕愈合能力的影响;Western blotting检测相关蛋白表达变化。  结果  与人胶质瘤细胞系U251和U373相比,U87细胞中ACC1表达较低;ACC1过表达抑制U87细胞增殖(P<0.01);ACC1过表达抑制U87细胞迁移、侵袭和划痕愈合能力(P<0.01);ACC1过表达迁移和侵袭相关蛋白波形蛋白(vimentin)、纤维连接蛋白(fibronectin)和尿激酶型纤溶酶原激活剂(uPA)表达下调(P<0.01),凋亡抑制蛋白Bcl-2和细胞周期蛋白(cyclin) B、cyclin D表达下调(P<0.01),p-STAT3蛋白表达下调(P<0.01),细胞周期蛋白P21表达上调(P<0.01)。  结论  过表达ACC1可能通过抑制STAT3活性,抑制人胶质瘤细胞的增殖、迁移和侵袭。

关键词: 乙酰辅酶A羧化酶1, U87细胞, 增殖, 迁移, 侵袭, 免疫印迹法,

Abstract:

Objective To explore the effect of acetyl-CoA carboxylase 1(ACC1) on cell proliferation, migration and invasion of human glioma cell line U87.   Methods  Western blotting was performed to examine endogenous ACC1 expression in human glioma cell lines U87, U251 and U373. ACC1 overexpression plasmid and the plasmid vector were transiently transfected into U87 cells. The level of ACC1 in control and ACC1 overexpression cells was examined by Western blotting. The effect of ACC1 on U87 cells migration and invasion was detected by Transwell assay. The effect of ACC1 on U87 cells scratch healing ability was detected by scratch test. The effect of ACC1 on U87 cells proliferation was investigated by MTT assay. Western blotting was conducted to detect the level changes of proteins.  Results  Among three human glioma cell lines U87, U251 and U373, endogenous ACC1 level in U87 cells was lower than that in other two cell lines. ACC1 overexpression inhibited U87 cell proliferation, as well as cell migration, invasion and scratch healing ability (P<0.05). Vimentin, fibronectin, urokinase type plasminogen activator (uPA), Bcl-2, cyclin B, cyclin D and p-STAT3 were down-regulated (P<0.05), P21 was up-regulated (P<0.05) after ACC1 overexpression.    Conclusion  These results suggest that ACC1 suppresses the proliferation, migration and invasion of human glioma cells, probably by inhibiting STAT3 activity.

Key words: Acetyl-CoA carboxylase 1, U87 cell, Proliferation, Migration, Invasion, Western blotting, Human

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