miR-590-5p mediates mitochondrial respiration, proliferation, and apoptosis in thyroid carcinoma cells via fibroblast growth factor receptor substrate 2.

OBJECTIVE: Thyroid carcinoma (TC) is the most common cancer of the endocrine system. Dysregulation of microRNA-590-5p (miR-590-5p) has been associated with various malignancies. Targeting mitochondrial respiration is beneficial in treating TC. This study aims to evaluate the role of miR-590-5p in the proliferation and apoptosis of TC cells via mediating mitochondrial respiration. MATERIALS AND METHODS: Reverse transcription quantitative polymerase chain reaction (qRT-PCR) was used to analyze differential expression of miR-590-5p in TC and para-cancerous tissues, normal thyrocytes, and TC cell lines. TC cells were transfected with agomiRNA negative control (agomiR-NC) or agomiRNA-590-5p (agomiR-590-5p). Cell counting kit 8 (CCK-8) assays, JC-1 staining, reactive oxygen species (ROS) measurements, and flow cytometry were used to detect cell proliferation, mitochondrial membrane potential (MMP), ROS levels, and apoptosis, respectively. The targeting relationship between miR-590-5p and fibroblast growth factor receptor substrate 2 (FRS2) was verified using dual-luciferase reporter assay. The role of miR-590-5p in tumor growth was analyzed in mouse xenograft tumors. RESULTS: miR-590-5p was expressed at low levels in TC tissues and cells relative to normal tissues. Overexpression of miR-590-5p reduced TC cell proliferation, enhanced apoptosis, and inhibited mitochondrial respiration. miR-590-5p suppressed FRS2 transcription in TC cells. Overexpression of FRS2 reversed the effects of miR-590-5p overexpression, limiting mitochondrial respiration and proliferation, and promoting apoptosis. In vivo, overexpression of miR-590-5p suppressed xenograft tumor growth in mice by reducing the transcription of FRS2. CONCLUSION: miR-590-5p was poorly expressed in TC. Overexpression of miR-590-5p limited TC cell proliferation and promoted apoptosis by reducing mitochondrial respiration via decreased transcription of FRS2.