PTEN gene expression inhibits proliferation and promotes apoptosis in human oral squamous carcinoma cell line TCA-8113

杨雨晗; 邓缅

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PTEN gene expression inhibits proliferation and promotes apoptosis in human oral squamous carcinoma cell line TCA-8113

更新时间：2026-01-09

- PTEN gene expression inhibits proliferation and promotes apoptosis in human oral squamous carcinoma cell line TCA-8113
- Journal of Army Medical University Vol. 33, Issue 14, Pages: 1484-1487(2011)
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  CLC： R739.85;R394.2;R730.23
- Published：2011
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杨雨晗,邓缅.PTEN基因调控口腔鳞癌细胞TCA-8113增殖及凋亡[J].陆军军医大学学报(原第三军医大学学报),2011,33(14):1484-1487.

　Yang Yuhan,Deng Mian.PTEN gene expression inhibits proliferation and promotes apoptosis in human oral squamous carcinoma cell line TCA-8113[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(14):1484-1487.
杨雨晗,邓缅.PTEN基因调控口腔鳞癌细胞TCA-8113增殖及凋亡[J].陆军军医大学学报(原第三军医大学学报),2011,33(14):1484-1487. DOI：

　Yang Yuhan,Deng Mian.PTEN gene expression inhibits proliferation and promotes apoptosis in human oral squamous carcinoma cell line TCA-8113[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(14):1484-1487. DOI：

摘要

目的评估PTEN基因在人口腔鳞癌细胞系TCA-8113中的增殖抑制和促凋亡功能。方法利用PTEN真核表达质粒转染TCA-8113细胞，另设PBS处理作为空白组，转染pcDNA3.1质粒和Lipofectamine处理作为对照组。采用MTT和克隆形成实验检测细胞增殖情况，采用流式细胞术、TUNEL和Western blot法检测细胞凋亡。结果 pcDNA3.1-PTEN转染TCA-8113细胞得到高效的外源性表达。克隆形成实验结果表明，空白组、Lipofectamine处理组、空载体质粒组和PTEN转染组的克隆数分别为（107.34±4.62）、（79.27±3.71）、（72.03±2.38）和（19.73±1.02），PTEN转染组抑制率为72.60%，与空载体质粒组相比，差异有统计学意义（P＜0.05）；MTT实验结果显示PTEN基因的表达对TCA-8113细胞的抑制率在48 h和72 h分别为18.16%和42.74%，PTEN转染组与空载体质粒组比较有统计学差异（P＜0.05）；流式细胞术检测结果显示，PTEN基因能引起62.12%的细胞死亡；TUNEL检测PTEN基因高表达能引起（45.67±2.31）%的细胞凋亡；Western blot检测结果表明，PTEN能抑制Bcl-2的表达并激活Bax的表达。结论 PTEN在TCA-8113细胞中的表达能显著抑制细胞增殖，促进细胞凋亡。

Abstract

Objective To evaluate the effects of PTEN gene expression on inhibiting the proliferation and promoting the apoptosis of human oral squamous carcinoma cell line TCA-8113. Methods TCA-8113 cells were transfected with eukaryotic expression plasmid pcDNA3.1-PTEN to obtain an experimental group. Besides

TCA-8113 cells were also treated with PBS

plasmid pcDNA3.1 and Lipofectamine to obtain a blank group and two control groups (a pcDNA3.1-transfected group and a Lipofectamine-treated group). The proliferation of TCA-8113 cells was detected by MTT assay and colony-forming assay. The apoptosis of TCA-8113 cells was evaluated by flow cytometry

TUNEL assay and Western blotting. Results TCA-8113 cells transfected with plasmid pcDNA3.1-PTEN had high intracellular expression of PTEN. Colony-forming assay showed that the clone numbers of the blank group

Lipofectamine-treated group

pcDNA3.1-transfected group and pcDNA3.1-PTEN-transfected group were 107.34±4.62

79.27±3.71

72.03±2.38 and 19.73±1.02

respectively. The inhibitive rate of TCA-8113 cells in the pcDNA3.1-PTEN-transfected group was 72.60%

significantly higher than that in the pcDNA3.1-transfected group (P＜0.05). MTT assay showed that the inhibitive rates of TCA-8113 cells in the pcDNA3.1-PTEN-transfected group were 18.16% and 42.74% at 48 h and 72 h after transfection

significantly higher than those in the pcDNA3.1-transfected group (P＜0.05). Flow cytometry showed that the death rate of TCA-8113 cells in the pcDNA3.1-PTEN-transfected group was 62.12%

significantly higher than that in the pcDNA3.1-transfected group (P＜0.05). TUNEL assay showed that the apoptosis of TCA-8113 cells in the pcDNA3.1-PTEN-transfected group was (45.67±2.31)%

significantly higher than that in the pcDNA3.1-transfected group (P＜0.05). Furthermore

PTEN inhibited Bcl-2 expression and activated Bax expression

as proven by Western blotting. Conclusion The expression of PTEN gene can remarkably inhibit the proliferation and promote the apoptosis of TCA-8113 cells.

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