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过表达RFX1对胶质瘤细胞增殖和侵袭的影响

程凯 张亚萍 曹丽 张晓延

中国肿瘤生物治疗杂志2018,Vol.25Issue(10):1021-1025,5.
中国肿瘤生物治疗杂志2018,Vol.25Issue(10):1021-1025,5.DOI:10.3872/j.issn.1007-385x.2018.10.008

过表达RFX1对胶质瘤细胞增殖和侵袭的影响

Effects of RFX1 over-expression on proliferation and invasion of glioma cells

程凯 1张亚萍 2曹丽 2张晓延3

作者信息

  • 1. 山西医科大学汾阳学院生物化学教研室,山西 汾阳 032200
  • 2. 山西医科大学汾阳学院科技中心,山西 汾阳 032200
  • 3. 山西医科大学汾阳学院病原生物学教研室,山西 汾阳 032200
  • 折叠

摘要

Abstract

Objective: To validate the effect and the possible mechanism of human regulatory factor X1 (RFX1) over-expression on the proliferation and invasion of glioma F98 cells. Methods: RFX1-overexpressed F98 cells (F98-RFX1 group) were constructed by lentivirus transfection, a control group (F98-Vector group) and normal group (F98 group) were established. The effect of RFX1 over-expression on F98 cell proliferation was observed with counting method, cell apoptosis was determined by AnnexinV-PI staining, and the cell invasion was observed with Transwell method. Results: F98 cell line over-expressing RFX1 was successfully established. The proliferation capacity of F98-RFX1 group was significantly lower than that of F98 group (48 h: [12.08±2.17]×104/ml vs [23.67±4.51]×104/ml, P<0.05] and F98-Vector group (96 h: [8.17±0.31]×104/ml vs [18.58±1.18]×104/ml, P<0.05); The apoptosis level of cells in F98-RFX1 group was significantly increased ([21.89±2.33]% vs [3.38±1.39]%, [10.42±1.83]%, P<0.05]; The invasiveness of cells in F98-RFX1 group was significantly reduced ([33.3±7.99] vs [56.5±13.9], [60.6±11.8], P<0.01). Conclusion: RFX1 can regulate the expression of genes related with proliferation and invasion, thereby inhibiting the proliferation and invasion ability of glioma cells and promote cell apoptosis.

关键词

恶性胶质瘤/F98细胞/调节因子X1 (RFX1)/增殖/侵袭/凋亡

Key words

malignant glioma/F98 cell line/regulatory factor X1 (RFX1)/proliferation/invasion/apoptosis

分类

医药卫生

引用本文复制引用

程凯,张亚萍,曹丽,张晓延..过表达RFX1对胶质瘤细胞增殖和侵袭的影响[J].中国肿瘤生物治疗杂志,2018,25(10):1021-1025,5.

基金项目

山西医科大学汾阳学院科技发展基金资助项目(No.2016B05) (No.2016B05)

中国肿瘤生物治疗杂志

OA北大核心CSCDCSTPCD

1007-385X

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