Lee Kyung-Jun, Singh Nitya, Bizuneh Michael, Kim Nam-Hyeok, Kim Hyeong Su, Kim Youngmi, Lee Jae-Jun, Kim Jung Han, Kim Jiye, Jeong Soo Young, Cho Hye-Yon, Park Sung Taek
Institute of New Frontier Research Team, Hallym University, Chuncheon 24252, Republic of Korea.
Division of Hemato-Oncology, Department of Internal Medicine, Kangnam Sacred-Heart Hospital, Hallym University Medical Center, Hallym University College of Medicine, Seoul 07441, Republic of Korea.
J Pers Med. 2023 Aug 25;13(9):1302. doi: 10.3390/jpm13091302.
(1) Background: To examine miR-429-meditated DEAD (Asp-Glu-Ala-Asp) box polypeptide 53 (DDX53) function in endometrial cancer (EC). (2) Methods: DDX53 and miR-429 levels were measured using quantitative real-time polymerase chain reaction and western blotting assays, cell invasion and migration using Transwell invasion and wound healing assays, and cell proliferation using colony-forming/proliferation assays. A murine xenograft model was also generated to examine miR-429 and DDX53 functions in vivo. (3) Results: DDX53 overexpression (OE) promoted key cancer phenotypes (proliferation, migration, and invasion) in EC, while in vivo, DDX53 OE hindered tumor growth in the murine xenograft model. Moreover, miR-429 was identified as a novel miRNA-targeting DDX53, which suppressed EC proliferation and invasion. (4) Conclusions: DDX53 and miR-429 regulatory mechanisms could provide novel molecular therapies for EC.
（1）背景：研究miR-429介导的DEAD（天冬氨酸-谷氨酸-丙氨酸-天冬氨酸）盒多肽53（DDX53）在子宫内膜癌（EC）中的作用。（2）方法：采用定量实时聚合酶链反应和蛋白质免疫印迹法检测DDX53和miR-429水平，采用Transwell侵袭实验和伤口愈合实验检测细胞侵袭和迁移能力，采用集落形成/增殖实验检测细胞增殖能力。还构建了小鼠异种移植模型以检测miR-429和DDX53在体内的功能。（3）结果：DDX53过表达（OE）促进了EC的关键癌症表型（增殖、迁移和侵袭），而在体内，DDX53 OE在小鼠异种移植模型中抑制了肿瘤生长。此外，miR-429被鉴定为一种靶向DDX53的新型微小RNA，它抑制了EC的增殖和侵袭。（4）结论：DDX53和miR-429的调控机制可为EC提供新的分子治疗方法。
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