MicroRNA-424 regulates epithelial-mesenchymal transition of endometrial carcinoma by directly targeting insulin-like growth factor 1 receptor.

Abstract:

:Although numerous miRNAs are reported to contribute to the carcinogenesis of malignant tumor, the specific role of miR-424 in endometrial carcinoma is seldom reported. To explore the effect of miR-424 on epithelial-mesenchymal transition and its underlying mechanism, we detected miR-424 expression in endometrial carcinoma tissue and cells. We found that miR-424 was significantly downregulated in endometrial carcinoma tissues and cells, especially in HEC-1B cells. To perform the functional analysis, we transfected HEC-1B with miR-424-mi, miR-424-inh, mi-control, and inh-control, respectively. We found that overexpression of miR-424 significantly decreases cell proliferation and migration, accompanied with the increased E-cadherin/Vimentin expression and the transition of mesenchymal to epithelial cell phenotype. We identified that insulin-like growth factor-1 receptor (IGF-1R) was a potential target of miR-424 by computational analysis followed by luciferase reporter assays. Of note, we found that the downregulation of miR-424 in HEC-1B cells enhanced endogenous IGF-1R expression. Further mechanistic analysis revealed that forced expression of IGF-1R in miR-424-mim transfected cells remedied the weakened migration resulting from overexpression of IGF-1R. Taken together, the results of the current study demonstrated that miR-424 was a tumor suppressor for endometrial carcinoma and a favorable factor against tumor progression through targeting IGF-1R, thus providing a target for the treatment of endometrial carcinoma.

journal_name

J Cell Biochem

authors

Shu S,Liu X,Xu M,Gao X,Fan J,Liu H,Li R

doi

10.1002/jcb.27528

subject

Has Abstract

pub_date

2018-09-06 00:00:00

eissn

0730-2312

issn

1097-4644

pub_type

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