OBJECTIVE: Thyroid cancer (TC) is one of the most common malignancies in the world. The prognosis of TC patients with advanced stage or recurrence is still poor. However, the biological role of miR-299-3p in TC remains unknown. The aim of our current research was to investigate the role of miR-299-3p in TC progression.
PATIENTS AND METHODS: MiR-299-3p expression level in both TC tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation ability was examined by Cell Count Kit-8 (CCK-8) assay and 5-ethynyl-2’-deoxyuridine (EdU) incorporation assay. Cell cycle progression and cell apoptosis were determined by flow cytometric analysis. Dual-Luciferase reporter assay was recruited to validate whether SHOC2 was a downstream target of miR-299-3p. In addition, the protein expression SHOC2 in transfected cells was examined by Western blotting.
RESULTS: We found that miR-299-3p was significantly downregulated in TC tissues and cell lines. To verify the role of miR-299-3p in TC, we transfected mimics and inhibitor in selected cell lines for over-expressing or down-expressing miR-299-3p, respectively. After transfection, cell functional experiments were subsequently employed. The results indicated that miR-299-3p could inhibit cell proliferation and cell cycle progression, whereas remarkably promote cell apoptosis in TC cell lines. Bioinformatics predicted that SHOC2 might be a potential target of miR-299-3p. Subsequent Dual-Luciferase reporter analysis validated our hypothesis. Rescue assay showed that miR-299-3p functioned as a tumor suppressor by targeting SHOC2 in TC.
CONCLUSIONS: MiR-299-3p functioned as a tumor suppressor in TC by targeting SHOC2. Our research provided novel insights into the molecular mechanism underlying TC progression, which might afford some new understanding in biomarkers and therapeutic strategies in TC development.Free PDF Download
To cite this article
X. Chen, M. Qi, Q. Yang, J.-Y. Li
MiR-299-3p functions as a tumor suppressor in thyroid cancer by regulating SHOC2
Eur Rev Med Pharmacol Sci
Vol. 23 - N. 1