Yan Weihong, Guo Hua, Suo Feng, Han Chunling, Zheng Hua, Chen Tong
Department of Pediatrics, Dongying People's Hospital, Dongying, Shangdong 257091, P.R. China.
Department of Radiology, Dongying People's Hospital, Dongying, Shangdong 257091, P.R. China.
Oncol Lett. 2017 Jan;13(1):151-154. doi: 10.3892/ol.2016.5395. Epub 2016 Nov 18.
The effect of miR-146a-dependent regulation of STAT1 on apoptosis in acute lymphoblastic leukemia (ALL) Jurkat cells was investigated. The miR-146a mimic and miR-146a inhibitor vectors were constructed , and experimental grouping was as follows: Control group (untreated Jurkat cells), empty vector group (Jurkat cells transfected with empty vector), agonist group (Jurkat cells transfected with miR-146a mimic) and the inhibitor group (Jurkat cells transfected with miR-146a inhibitor). Western blot analysis was used to observe the expression, respectively, of STAT1, p-STAT1 and Bcl-xL, and flow cytometry was used to test apoptosis in Jurkat cells. STAT1 and p-STAT1 expression in the agonist group was higher than that in the control and empty vector groups, but lower in the inhibitor group, and differences were statistically significant (P<0.05). The rate of apoptosis in the agonist group was significantly higher than that of the control group and blank vector group, and it was significantly lower in the inhibitor group (P<0.05). As a tumor suppressor, miR-146a can regulate expression of apoptosis-promoting factor STAT1, and anti-apoptosis factor Bcl-xL, and is able to promote apoptosis of ALL Jurkat cells.
研究了miR-146a依赖性调控信号转导和转录激活因子1(STAT1)对急性淋巴细胞白血病(ALL)Jurkat细胞凋亡的影响。构建了miR-146a模拟物和miR-146a抑制剂载体,实验分组如下:对照组(未处理的Jurkat细胞)、空载体组(转染空载体的Jurkat细胞)、激动剂组(转染miR-146a模拟物的Jurkat细胞)和抑制剂组(转染miR-146a抑制剂的Jurkat细胞)。采用蛋白质免疫印迹分析分别观察STAT1、磷酸化STAT1(p-STAT1)和Bcl-xL的表达,采用流式细胞术检测Jurkat细胞凋亡情况。激动剂组中STAT1和p-STAT1的表达高于对照组和空载体组,但低于抑制剂组,差异具有统计学意义(P<0.05)。激动剂组的凋亡率显著高于对照组和空载体组,而抑制剂组则显著降低(P<0.05)。作为一种肿瘤抑制因子,miR-146a可调控促凋亡因子STAT1和抗凋亡因子Bcl-xL的表达,并能够促进ALL Jurkat细胞凋亡。