RETRACTED: MicroRNA-641 Inhibits Endometrial Cancer Progression via Targeting AP1G1 (Retracted Article)

被引:2
|
作者
Dong, Yanfen [1 ]
Yang, He [2 ]
Hua, Handan [2 ]
机构
[1] Nanjing Med Univ, Affiliated Changzhou Peoples Hosp 2, Dept Lab, Changzhou 213003, Peoples R China
[2] Nanjing Med Univ, Affiliated Changzhou Peoples Hosp 2, Dept Gynecol, Changzhou 213003, Peoples R China
关键词
MESENCHYMAL TRANSITION; CELLS; PI3K/AKT; BIOMARKERS; PATHWAY;
D O I
10.1155/2022/7918596
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
MicroRNA-641 (miR-641) was significantly decreased in various cancers, but its roles in endometrial cancer (EC) remain unclear. We explored the influences of miR-641 on the EC cells. In our study, the miR-641 expression was reduced in EC cells. Overexpression of miR-641 inhibited viability and proliferation of HEC-1A and HECCL-1 cells by CCK-8 and colony formation assays. Additionally, flow cytometry revealed that overexpression of miR-641 could remarkably promote apoptosis and arrest the cell cycle at the G1 phase of HEC-1A and HECCL-1 cells. Besides, forced expression of miR-641 suppressed the migration and invasion of HEC-1A and HECCL-1 cells as evidenced by wound healing and transwell assay. Moreover, AP1G1 was confirmed as a target gene of miR-641 by StarBase prediction and DLR assay and their expressions were negatively correlated. Overexpression of AP1G1 neutralized the roles of miR-641 mimic on the viability, proliferation, apoptosis, and migration of HEC-1A and HECCL-1 cells. Our findings illustrated that miR-641 was reduced in the EC cells and AP1G1 antagonized the miR-641 mimic-induced inhibition of the EC progression in vitro. Therefore, miR-641 may emerge as an effective molecule for EC treatment.
引用
收藏
页数:9
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