期刊
EXPERIMENTAL AND THERAPEUTIC MEDICINE
卷 21, 期 6, 页码 -出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2021.10084
关键词
differentiated thyroid cancer; microRNA-221; microRNA-222; suppressor of cytokine signaling 3; solute carrier family 5 member 5; radiosensitivity
资金
- National Natural Science Foundation of China [81502318]
- Zhejiang Province Natural Science Foundation of China [LY20H180007]
The expression levels of miR-221-3p and miR-222-3p are upregulated in thyroid cancer, while SOCS3 is downregulated. Overexpression of miR-221-3p and miR-222-3p leads to decreased expression of SOCS3, E-cadherin, and NIS, and increased expression of phosphorylated STAT3 and vimentin in thyroid cancer cells.
The expression levels of microRNA (miR)-221-3p and miR-222-3p in thyroid cancer have been found to be upregulated compared with those in normal tissues. The present study aimed to determine the effects and potential underlying mechanisms of miR-221-3p and miR-222-3p on the regulation of radioactive iodine (I-131) uptake and radiosensitivity of thyroid cancer cells. The potential regulatory target genes of miR-221-3p and miR-222-3p were predicted by bioinformatics analysis, and reverse transcription-quantitative polymerase chain reaction was used to verify miR-221-3p, miR-222-3p and target gene expression levels in thyroid cancer tissues and cell lines. Overexpression of miR-221-3p or miR-222-3p in cell models was performed using lentivirus infection. Knockdown of miR-221-3p and miR-222-3p in cells was achieved using oligonucleotide inhibitor transfection. Western blotting was used to analyze the expression levels of target proteins. In addition, the effects of miR-221-3p and miR-222-3p on the radiosensitivity of thyroid cancer cells were verified using a colony formation assay. The results of the present study revealed that the expression levels of miR-221-3p and miR-222-3p were significantly upregulated, while the expression levels of suppressor of cytokine signaling 3 (SOCS3) were downregulated in thyroid cancer tissues. Furthermore, miR-221-3p and miR-222-3p overexpression downregulated the expression levels of SOCS3, E-cadherin and solute carrier family 5 member 5 (NIS), and upregulated the expression levels of phosphorylated STAT3 and vimentin. Following the overexpression of miR-221-3p or miR-222-3p in the FTC133 and TPC1 cell lines, their radiosensitivity was suppressed. In conclusion, the findings of the present study suggested that miR-221-3p and miR-222-3p may downregulate the expression levels of NIS and promote radioresistance. The potential mechanism was hypothesized to be associated with the miR-221-3p and miR-222-3p targeting of the SOCS3 gene, which may subsequently activate the STAT3 signaling pathway.
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