Retracted: MicroRNA-373 promotes the development of endometrial cancer by targeting LATS2 and activating the Wnt/β-Catenin pathway

In the female reproductive tract, endometrial cancer is the most common malignant tumor. Recently, the specific functions of many miRNAs have been identified in endometrial cancer. However, the contradictory effects of microRNA-373 (miR-373) in different human cancers draw our attention. In the pres...

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Bibliographic Details
Published in:Journal of cellular biochemistry 2019-05, Vol.120 (5), p.8611-8618
Main Authors: Li, Yan, Sun, Dongxia, Gao, Jie, Shi, Zhimin, Chi, Pengyu, Meng, Yuanyuan, Zou, Changjun, Wang, Yanhua
Format: Article
Language:English
Subjects:
Cancer
Catenin
Cell migration
Cell proliferation
Endometrial cancer
Endometrium
Hormone replacement therapy
Kinases
MicroRNAs
miRNA
Reproductive system
Ribonucleic acid
RNA
Tumor suppressor genes
Tumors
Wnt protein
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Summary:In the female reproductive tract, endometrial cancer is the most common malignant tumor. Recently, the specific functions of many miRNAs have been identified in endometrial cancer. However, the contradictory effects of microRNA-373 (miR-373) in different human cancers draw our attention. In the present research, upregulation of miR-373 was identified in endometrial cancer which predicted poor prognosis. Moreover, upregulation of miR-373 promoted the migration, invasion, and proliferation of endometrial cancer cells. To further confirm that results, the EMT and Wnt/β-Catenin pathways were also investigated, which were promoted by overexpression of miR-373. Then, we further investigate the downstream factor, large tumor suppressor kinase 2 (LATS2) which was inhibited by miR-373. LATS2 was verified as a direct target gene of miR-373 through luciferase reporter assay. Especially, the facilitation of miR-373 for cell proliferation, migration and invasion was impaired by LATS2. Taken together, miR-373 promotes the progression of endometrial cancer through targeting LATS2 and promoting EMT and Wnt/β-Catenin pathway.
ISSN:0730-2312
1097-4644
DOI:10.1002/jcb.28149