MicroRNA-188-5p Promotes Epithelial–Mesenchymal Transition by Targeting ID4 Through Wnt/β‑catenin Signaling in Retinoblastoma

Abstract

Purpose

Here, we investigated the involvement of the miR-188-5p/inhibitor of the DNA binding 4 (ID4) axis in retinoblastoma (Rb).

Patients and methods

We included 35 Rb tissues and the corresponding adjacent normal tissues. RT-qPCR, Western blot, lentivirus transfection, measurement of cell migration in vitro, and chip analysis were performed during the study. Mouse Rb models were established to investigate the in vivo mechanisms.

Results

We showed that miR-188-5p was upregulated in Rb tissues; moreover, we identified a pathway involving the upregulation of miR-188-5p and its downstream target, ID4, in vitro. Cell experiments revealed that the overexpression of miR-188-5p significantly downregulated the expression of ID4 and the underlying mechanism involved direct targeting of the ID4 3′-UTR. The levels of ID4 are lower in Rb tissues; it plays an antitumor role by inhibiting Rb metastasis in vitro and in vivo. Further investigation revealed that the miR-188-5p/ID4 axis regulated metastasis by promoting epithelial–mesenchymal transition (EMT). We demonstrated that microRNA-188-5p promoted EMT by targeting ID4 through Wnt/β catenin signaling in Rb.

Conclusion

miRNA-188-5p can promote EMT by targeting ID4 through the Wnt/β‑catenin signaling pathway.