MicroRNA-584-5p Restrains the Viability of Lung Cancer Cells through Targeting DPY30 Directly

被引:0
|
作者
Su, Jing [1 ]
Lin, Xiushan [2 ]
Zhao, Jianqing [1 ]
Zhang, Ning [1 ]
Wang, Jingjing [1 ]
Shan, Lin [3 ]
机构
[1] Hebei North Univ, Affiliated Hosp 1, 12 Changqing Rd, Zhangjiakou, Hebei, Peoples R China
[2] Hainan Med Univ, Dept Resp Med, Affiliated Hosp 1, 31 Longhua Rd, Haikou, Hainan, Peoples R China
[3] Shanghai Huadong Hosp, Resp Med, 221 Yan West Rd, Shanghai 200040, Peoples R China
关键词
Cell Viability; Dpy-30 Histone Methyltransferase Complex Regulatory Subunit; Ki67; MicroRNA-584-5p; Proliferating Cell Nuclear Antigen; INVASION;
D O I
10.31901/24566330.2022/22.03.818
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Dysregulation of microRNAs (miRNAs) in lung cancer participates in lung cancer progression. This study was focused on investigating regulatory mechanism of miR-584-5p in lung cancer cells. Differential miR-584-5p and DPY30 expressions in samples of lung carcinoma were evaluated using ENCORI and GEPIA (http://gepia.cancer-pku.cn/). Using RT-qPCR, miR-584-5p was detected to be downregulated in lung cancer cells. MiR-584-5p overexpression inhibited H460 cell viability and suppressing Ki67 and PCNA protein expressions. Moreover, DPY30 was found to be targeted by miR-584-5p using luciferase reporter test, which was upregulated in lung cancer cells. Furthermore, overexpressed DPY30 restrained effects of miR-584-5p mimics, causing accelerated H460 cell viabilities and upregulated Ki67 and PCNA protein expressions. In H460 cells, miR-594-5p suppressed cell viability and inhibited protein expressions of Ki67 and PCNA through binding DPY30.
引用
收藏
页码:206 / 214
页数:9
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