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

MicroRNAs (miRNAs) are frequently dysregulated in human cancers and can act as potent oncogenes or tumor suppressor genes. Aberrant expression of miR-424 has been identified in some types of cancer, however, its expression and potential biologic role in endometrial cancer are remains to be determined. In the present study, we demonstrated that miR-424 was downregulated in human endometrial cancer and suppressed growth of the human Ishikawa and HEC-1B endometrial cancer cell lines. Bioinformatics analysis indicated that E2F7 was a putative target of miR-424. In a luciferase reporter system, we confirmed that E2F7 was a direct target gene of miR-424. Furthermore, knockdown of E2F7 inhibited Ishikawa and HEC-1B cell growth. These findings indicate that miR-424 targets the E2F7 transcript and suppresses endometrial cancer cell growth, suggesting that miR-424 has a tumor suppressive role in human endometrial cancer pathogenesis.
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PMID:MicroRNA-424 may function as a tumor suppressor in endometrial carcinoma cells by targeting E2F7. 2570 47

Our previous study explored the roles of microRNA-424 (miR-424) in the development of endometrial carcinoma (EC) and analyzed the miR-424/E2F7 axis in EC cell growth. In this study, we investigated the status of miR-424 in human endometrial cancer tissues, which were collected from a cohort of Zunyi patients. We found that the expression level of miR-424 was associated with clinical tumor stage, cell differentiation, lymph node metastasis and cell migration ability. Cell function experiments demonstrated that miR-424 overexpression suppressed the invasion and migration abilities of endometrial carcinoma cells in vitro. Bioinformatic predictions and dual-luciferase reporter assays suggested E2F6 as a possible target of miR-424. RT-PCR and western blot assays demonstrated that miR-424 transfection reduced the expression level of E2F6, while inhibiting miR-424 with ASO-miR-424 (antisense oligonucleotides of miR-424) increased the expression level of E2F6. Cell function experiments indicated that E2F6 transfection rescued the EC cell phenotype induced by miR-424. In addition, we also found that E2F6 negatively regulated miR-424 expression in EC cells. In summary, our results demonstrated that the miR-424/E2F6 feedback loop modulates cell invasion, migration and EMT in EC and that the miR-424/E2Fs regulation network may serve as a new and potentially important therapeutic target in EC.
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PMID:MicroRNA-424/E2F6 feedback loop modulates cell invasion, migration and EMT in endometrial carcinoma. 2937 86