Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endometrial carcinoma (EC) is one of the most common malignancies of female reproductive tract in developed countries. MicroRNA is frequently dysregulated in human cancers and acts a key regulator role in tumor cell growth and metastasis. The aims of this study were to investigate the roles of microRNA-184 (miR-184) in EC cells and to identify its potential molecular mechanism. Here, the data revealed that miR-184 was significantly downregulated in human EC tissue compared with normal endometrial tissue, and the level of miR-184 expression was associated with lymph node metastasis and prognosis in patients with EC. In vitro assays, overexpression of miR-184 could suppress the proliferation and invasion of HEC-1B and RL95-2 cells. Moreover, bioinformatics analysis showed that cell division cycle 25A (CDC25A) was a putative target gene of miR-184. Dual luciferase reporter assay confirmed that miR-184 significantly downregulated CDC25A expression via directly interaction with the putative binding site in the 3'-untranslated region (3'-UTR) of CDC25A mRNA. Interestingly, knockdown of CDC25A resulted in inhibition of HEC-1B and RL95-2 cells growth and invasion. Mechanistic investigation revealed that downregulation of the Notch receptors (NOTCH1, NOTCH2, NOTCH3 and NOTCH4) and target gene HES1 by miR-184 could be reversed by CDC25A overexpression. In summary, our data demonstrate that CDC25A is a target gene of miR-184 in EC cells, and decreased expression of miR-184 suppresses the growth and invasion of EC cells via CDC25A-dependent Notch signaling pathway, suggesting that miR-184 may be a promising target for a new therapeutic strategy against EC.
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PMID:Decreased expression of miR-184 restrains the growth and invasion of endometrial carcinoma cells through CDC25A-dependent Notch signaling pathway. 3089 77