The Effect of MicroRNA-92a (miR-92a) on Non-Small Cell Lung Cancer (NSCLC) Cell Biological Behaviors and Janus Protein-Tyrosine Kinase 1 (JAK1)/Signal Transducer and Activator of Transcription (STAT3) Signaling

被引:1
|
作者
Yi, Jianghong [1 ]
Zhao, Jie [2 ]
Xiao, Pengfei [3 ]
Gao, Minghui [3 ]
机构
[1] Brain Hosp Hunan Prov, Dept Crit Med, Changcha 410000, Hunan, Peoples R China
[2] Brain Hosp Hunan Prov, Dept Rehabil Med, Changcha 410000, Hunan, Peoples R China
[3] Brain Hosp Hunan Prov, Dept Oncol, Changcha 410000, Hunan, Peoples R China
关键词
NSCLC; miR-92a; JAK1/STAT3; Signal; A549; Cells; PATHWAY; GROWTH;
D O I
10.1166/jbt.2021.2715
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Our study investigates miR-92a's effect on the biological behaviors of non-small cell lung cancer (NSCLC) cells and Janus protein-tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) signal transduction. A549 cells were divided into KB group (no transfection), NC group (negative control transfection), and SY group (transfection with miR-92a inhibitor) followed by analysis of the expression of miR-92a, JAK1, and STAT3 by qRT-PCR, cell proliferation, invasion and apoptosis as well as JAK1/STAT3 protein expression. The miR-92a, JAK1, and STAT3 expression in SY group were significantly lower than NC group and KB group (P < 0.05), indicating the successful transfection. The A549 cell proliferation in SY group was significantly decreased compared with NC and KB group (P < 0.05). Cell apoptosis rate in SY group was 25.23 +/- 2.31%, which was significantly higher than that in NC (8.15 +/- 0.82%) and KB group (8.08 +/- 0.79%). The number of cell invasion in SY group was significantly reduced (88.6 +/- 7.32) compared with NC group (189.71 +/- 15.37) and KB group (181.32 +/- 14.62) (F = 937.8, P < 0.001). SY group showed significantly lower JAK1/STAT3 protein expression than NC and KB group. In conclusion, silencing miR-92a can inhibit proliferation, migration, and invasion of A549 cells, which may be related to JAK1/STAT3 signaling pathway.
引用
收藏
页码:1582 / 1587
页数:6
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