Overexpression of activating transcription factor 3 exerts suppressive effects in HepG2 cells
Overexpression of activating transcription factor 3 exerts suppressive effects in HepG2 cells
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DOI：
10.3892/mmr.2018.9707
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发表时间：
2019-02-01
影响因子：
3.4
通讯作者：
Huang, Aimin
中科院分区：
文献类型：
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作者：
Li, Xiaoyan;Zang, Shengbing;Huang, Aimin
本研究观察并比较了HepG2细胞在激活转录因子3（ATF3）过度表达之前和之后的生物学行为。还进行了研究 ATF3 影响肝癌细胞的细胞学功能的实验。采用MTT、Transwell和流式细胞术观察检测慢病毒（LV）-ATF3增强绿色荧光蛋白（EGFP）感染和未感染的HepG2细胞的生物学行为。评估ATF3过表达对细胞增殖、迁移、凋亡和细胞周期进程的影响。成功构建LV-ATF3-EGFP过表达载体，并成功感染HepG2细胞。 ATF3过表达后,细胞增殖减少,细胞凋亡率加快,细胞周期进程减慢(P<0。05),但有逐渐减少的趋势。总之，ATF3 在 HepG2 细胞中发挥抑制作用，可能是通过抑制癌细胞生长、加速细胞凋亡和阻断细胞周期进程来实现的。针对 ATF3 表达的干预可能代表了预防和治疗人类肝癌的新方法。
The present study observed and compared the biological behaviour of HepG2 cells prior and subsequent to the overexpression of activating transcription factor 3 (ATF3). Experiments investigating the cytological function by which ATF3 affects liver cancer cells were also performed. MTT, Transwell and flow cytometry assays were used to observe and detect the biological behaviour of HepG2 cells with and without lentivirus (LV)-ATF3-enhanced green fluorescent protein (EGFP) infection. The effects of ATF3 overexpression on cell proliferation, migration, apoptosis and cell cycle progression were evaluated. The LV-ATF3-EGFP overexpression vector was successfully constructed, and the HepG2 cells were successfully infected with the vector. Following ATF3 overexpression, cell proliferation was decreased, the rate of cell apoptosis was accelerated and cell cycle progression was slowed (P0.05), although there was a trend towards a gradual decrease. In conclusion, ATF3 exerted suppressive effects in HepG2 cells, potentially by inhibiting cancer cell growth, accelerating cell apoptosis, and blocking cell cycle progression. Intervention targeting ATF3 expression may represent a novel approach for the prevention and treatment of human liver cancer.