BTG1对喉癌细胞增殖和凋亡的影响及其机制研究

姜润学; 胡万宁; 孙国贵

doi:10.3969/j.issn.1007-3969.2015.12.007

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BTG1对喉癌细胞增殖和凋亡的影响及其机制研究

更新时间：2025-12-31

- BTG1对喉癌细胞增殖和凋亡的影响及其机制研究
- The effect of BTG1 overexpression on the proliferation and apoptosis of laryngeal cancer cells and its molecular mechanism in vitro
- 中国癌症杂志 2015年25卷第12期页码：959-965
- 作者机构：
  
  1. ．河北联合大学附属唐山市人民医院头颈外科,河北,唐山,063000
  2. ．河北联合大学附属唐山市人民医院放化疗科,河北,唐山,063000
- 作者简介：
- 基金信息：
- DOI：10.3969/j.issn.1007-3969.2015.12.007
  中图分类号：
- 网络出版：2016-02-03，
  
  纸质出版：2015-02-03
- 稿件说明：
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姜润学,胡万宁,孙国贵,等. BTG1对喉癌细胞增殖和凋亡的影响及其机制研究[J]. 中国癌症杂志, 2015, 25(12): 959-965.

姜润学, 胡万宁, 孙国贵. The effect of BTG1 overexpression on the proliferation and apoptosis of laryngeal cancer cells and its molecular mechanism in vitro[J]. China Oncology, 2015, 25(12): 959-965.
姜润学,胡万宁,孙国贵,等. BTG1对喉癌细胞增殖和凋亡的影响及其机制研究[J]. 中国癌症杂志, 2015, 25(12): 959-965. DOI： 10.3969/j.issn.1007-3969.2015.12.007.

姜润学, 胡万宁, 孙国贵. The effect of BTG1 overexpression on the proliferation and apoptosis of laryngeal cancer cells and its molecular mechanism in vitro[J]. China Oncology, 2015, 25(12): 959-965. DOI： 10.3969/j.issn.1007-3969.2015.12.007.

摘要

背景与目的：在多种细胞中B细胞易位基因1(B-cell translocation gene 1，BTG1)能够抑制细胞增殖，促进细胞凋亡，调节细胞周期进程及分化。该研究通过体外实验探讨BTG1高表达对喉癌Hep-2细胞增殖、凋亡及细胞周期的影响及其相关作用机制。方法：构建pEGFP-N1-BTG1，培养并转染喉癌Hep-2细胞，分为实验组(转染pEGFP-N1-BTG1的Hep-2细胞)和对照组(转染pEGFP-N1空质粒的Hep-2细胞)。采用蛋白［质］印迹法(Western blot)检测两组细胞中BTG1蛋白的表达水平；应用MTT法检测细胞的增值活性；使用流式细胞术检测细胞周期分布和磷脂酰丝氨酸外翻分析(Annexin Ⅴ-FITC/PI)检测细胞凋亡；采用Western blot法检测细胞周期调控蛋白Cyclin D1、凋亡相关蛋白Bcl-2表达情况。结果：成功构建pEGFP-N1-BTG1，Western blot检测结果显示，实验组细胞中BTG1蛋白表达水平明显高于对照组细胞(0.921±0.091 vs 0.308±0.047，P0.05)。实验组与对照组细胞相比，从第24 h实验组细胞生长速度减慢，细胞增值能力降低，两组比较差异有统计学意义(P0.05)；实验组细胞中Cyclin D1蛋白表达水平下降(0.436±0.023 vs 0.916±0.092，P0.05)，细胞周期的G

期细胞比例升高［(85.1±5.2)% vs (63.8±3.1)%，P0.05)］；S期细胞比例降低［(8.3±1.1)% vs(23.1±1.5)%，P0.05］；实验组细胞Annexin Ⅴ增多，细胞早期凋亡率升高［(10.3±1.1)% vs (2.8±0.3)%，P0.05］，抗凋亡蛋白Bcl-2表达水平降低(0.167±0.009 vs 0.834±0.084，P0.05)。结论：BTG1高表达能明显抑制喉癌Hep-2细胞的生长增殖、诱导凋亡，其可能的机制与BTG1参与细胞周期调控、诱导细胞凋亡相关。

Abstract

Background and purpose: B-cell translocation gene 1(BTG1) can inhibit cell proliferation

promote cell apoptosis and regulate cell cycle progression and differentiation in a variety of cell types. This study aimed to explore the influence on cell proliferation

apoptosis and cell cycle

and its related mechanism of laryngeal cancer Hep - 2 cell lines through BTG1 overexpression by in vitro experiments. Methods: The BTG1 expression plasmids were constructed and transfected into Hep-2. They were divided into experimental group (transfected BTG1 of Hep-2 cells) and control group (transfected empty plasmid of Hep-2 cells). Western blot method was used to identify BTG1 protein expression levels of cells; proliferation activity of cells was detected by MTT assay; flow cytometry was used to analyze the cell cycle distribution and Annexin Ⅴ-FITC/PI cell apoptosis; Western blot was also used to assay cell cycle regulatory protein and apoptosis-related protein expression. Results: The pEGFP-N1-BTG1 plasmid was constructed successfully

and the expression of BTG1 protein was higher in experimental group than that in control group (0.921±0.091 vs 0.308±0.047

P0.05). Compared with the two group of laryngeal cancer Hep-2 cells

the cell growth in experimental group was slowed down and the proliferation was reduced (P0.05); Cyclin D1 protein expression level was decreased (0.436±0.023 vs 0.916±0.092

P0.05)

the proportion of G

phase cell cycle was increased [(85.1±5.2)% vs (63.8±3.1)%

P0.05

]

the proportion of S phase cell was decreased [(8.3±1.1)% vs (23.1±1.5)%

P0.05

]

phosphatidylserine ectropion in experimental group was increased

cell early apoptosis was significant [(10.3±1.1)% vs (2.8±0.3)%

P0.05

]

and anti-apoptotic protein Bcl-2 expression level was reduced(0.167±0.009 vs 0.834±0.084

P0.05). Conclusion: BTG1 high expression could inhibit the proliferation growth of laryngeal Hep-2 cells and promote its apoptosis

and the possible mechanisms are interrelated with BTG1 involved in cell cycle regulation and causing cell apoptosis.

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