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

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

  • Arch Endocrinol Metab. 2025 Aug 20;69(4):e240410. doi: 10.20945/2359-4292-2024-0410.
Penghui Wang 1 2,  Xiaoli Hou 3,  Wei Sun 4,  Jiajie Chen 4,  Yasen Cao 4,  Hong Cheng 4
Affiliations

Affiliations

  • 1 Yangzhou University Medical College Yangzhou China Yangzhou University Medical College, Yangzhou, China.
  • 2 Affiliated Hospital of Yangzhou University Department of Clinical Laboratory Yangzhou China Department of Clinical Laboratory, Affiliated Hospital of Yangzhou University, Yangzhou, China.
  • 3 Yangzhou Polytechnic College Department of Medical Science Yangzhou China Department of Medical Science, Yangzhou Polytechnic College, Yangzhou, China.
  • 4 Yangzhou University Institute of Translational Medicine Yangzhou University Medical College Yangzhou China Yangzhou University Medical College, Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research, Institute of Translational Medicine, Yangzhou University, Yangzhou, China.
PMID: 40834280 DOI: 10.20945/2359-4292-2024-0410
Abstract

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.

Keywords

FRS2; Thyroid carcinoma; cell proliferation; miR-590-5p; mitochondrial respiration.

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