MiR-663a Inhibits Radiation-Induced Epithelium-to-Mesenchymal Transition by Targeting TGF-β1

Area of Science:

• Molecular Biology
• Cell Biology
• Radiation Oncology

Background:

• MicroRNA-663a (miR-663a) is implicated in radiation responses and the radiation-induced bystander effect.
• Epithelium-to-mesenchymal transition (EMT) is a critical process in development and disease, often influenced by radiation.
• The precise role of miR-663a in radiation-induced EMT requires further elucidation.

Purpose of the Study:

• To investigate the function of miR-663a in the context of radiation-induced EMT.
• To determine the molecular mechanisms underlying miR-663a's involvement in radiation-induced EMT.

Main Methods:

• Epithelium-to-mesenchymal transition (EMT) was induced using TGF-β1 or irradiation (IR).
• miR-663a transfection was performed, followed by assessments of cell migration and morphology.
• Expression levels of miR-663a, TGF-β1, and EMT markers were quantified.

Main Results:

• miR-663a transfection suppressed TGF-β1- or IR-induced enhancement of cell migration and mesenchymal characteristics.
• Both X-ray and carbon ion irradiation upregulated TGF-β1 and downregulated miR-663a.
• miR-663a-mediated silencing of TGF-β1 reversed radiation-induced EMT.

Conclusions:

• miR-663a exerts an EMT-suppressing effect in radiation-induced EMT.
• The mechanism involves the modulation of TGF-β1 signaling by miR-663a.
• miR-663a represents a potential therapeutic target for managing radiation-induced EMT.