MicroRNA-19a inhibits nasopharyngeal carcinoma CNE1 cells viability and migration, but induces apoptosis by inhibition of Bcl-2

被引:0
|
作者
Xu, Hongbin [1 ]
Li, Long [1 ]
Wu, Yuan [1 ]
He, Haicui [1 ]
Hu, Desheng [1 ]
机构
[1] Hubei Canc Hosp, Dept Radiat Oncol, 116 South Zhuodaoquan Rd, Wuhan 430079, Peoples R China
关键词
MicroRNA-19a; nasopharyngeal carcinoma; viability; migration; apoptosis; Bcl-2; NF-KAPPA-B; TUMOR-GROWTH; LUNG-CANCER; RADIOSENSITIVITY; PROLIFERATION; SUPPRESSION; INVASION; PATHWAY; MIR-19A;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer, frequently occurring in Southeast Asia and Southern China. Several microRNAs (miRNAs) have been shown to have an inhibitory effect on NPC, whereas the effect of miR-19a on NPC remains unclear. In this study, an effort has been made to study the potential effect of miR-19a on NPC cell viability, migration and apoptosis. Human NPC CNE1 cells were transfected with miR-19a mimic, miR-19a inhibitor, Bcl-2 targeted small interfering RNA (siRNA) and corresponding controls, respectively. RT-qPCR and western blot were performed to determine the expressions of miR-19a at mRNA and protein levels. Subsequently, cell viability, migration and apoptosis of the transfected cells were analyzed by Cell Counting Kit-8 (CCK-8), Transwell and flow cytometry assays. Analysis of signaling pathways were detected by western blot. Results showed that miR-19a overexpression inhibited cell viability and migration but promoted apoptosis in CNE1 cells (P < 0.05 or P < 0.001). Bcl-2 was negatively regulated by miR-19a, and Bcl-2 silence could dramatically induce apoptosis, and abolish miR-19a suppression induce increases in cell viability and migration (P < 0.05 or P < 0.01 or P < 0.001). Besides, Bcl-2 silence abolished miR-19a suppression induced activation of p38MAPK, p65 and I.Ba. These results indicated that miR-19a inhibited cell viability, migration and induced apoptosis by down-regulating Bcl-2 in NPC cells.
引用
收藏
页码:7261 / 7269
页数:9
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