期刊
INTERNATIONAL JOURNAL OF HUMAN GENETICS
卷 22, 期 3, 页码 206-214出版社
KAMLA-RAJ ENTERPRISES
DOI: 10.31901/24566330.2022/22.03.818
关键词
Cell Viability; Dpy-30 Histone Methyltransferase Complex Regulatory Subunit; Ki67; MicroRNA-584-5p; Proliferating Cell Nuclear Antigen
资金
- Key project of Medical science research in Hebei Province [20160366]
This study revealed that miR-584-5p is downregulated and DPY30 is upregulated in lung cancer cells. Overexpression of miR-584-5p inhibits cell viability and protein expressions of Ki67 and PCNA. DPY30 is targeted by miR-584-5p and overexpressed DPY30 attenuates the effects of miR-584-5p.
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.
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