Dong Yanfen, Yang He, Hua Handan
Department of Laboratory, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Department of Gynecology, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Evid Based Complement Alternat Med. 2022 Sep 30;2022:7918596. doi: 10.1155/2022/7918596. eCollection 2022.
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 . Therefore, miR-641 may emerge as an effective molecule for EC treatment.
微小RNA-641（miR-641）在多种癌症中显著降低，但其在子宫内膜癌（EC）中的作用仍不清楚。我们探讨了miR-641对EC细胞的影响。在我们的研究中，EC细胞中miR-641表达降低。通过CCK-8和集落形成试验，miR-641的过表达抑制了HEC-1A和HECCL-1细胞的活力和增殖。此外，流式细胞术显示，miR-641的过表达可显著促进HEC-1A和HECCL-1细胞凋亡，并使细胞周期停滞在G1期。此外，伤口愈合试验和transwell试验证明，miR-641的强制表达抑制了HEC-1A和HECCL-1细胞的迁移和侵袭。此外，通过StarBase预测和双荧光素酶报告试验证实AP1G1是miR-641的靶基因，且它们的表达呈负相关。AP1G1的过表达抵消了miR-641模拟物对HEC-1A和HECCL-1细胞活力、增殖、凋亡和迁移的作用。我们的研究结果表明，EC细胞中miR-641降低，AP1G1拮抗miR-641模拟物诱导的EC进展抑制。因此，miR-641可能成为EC治疗的有效分子。
