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Archive > Volume 33 Issue 8 > 2026,33(8):857-866. DOI:10.3872/j.issn.1007-385X.2026.08.006 Prev Next
Basic Research
miR-532-3p targets DDOST and inhibits thyroid cancer TPC-1 cell proliferation, glycolysis, and xenograft tumor growth in nude mice
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Abstract:
Objective: This study aimed to investigate the effects of miR-532-3p on thyroid cancer TPC-1 cell proliferation and glycolysis and to preliminarily explore the underlying mechanism by targeting dolichyl-diphosphooligosaccharide protein glycosyltransferase non-catalytic subunit (DDOST). Methods: The basal expression of miR-532-3p was assessed in normal thyroid Nthy-ori 3-1 cells and thyroid cancer cell lines TPC-1, FTC-133, and IHH-4. TPC-1 cells were selected for subsequent experiments and divided into mimic-NC group, miR-532-3p mimic group, inhibitor-NC group, miR-532-3p inhibitor group, mimic-NC + pcDNA-NC group, mimic-NC+pcDNA-DDOST group, miR-532-3p mimic + pcDNA-NC group, and miR-532-3p mimic + pcDNA-DDOST group. The targeting relationship between miR-532-3p and DDOST was detected by dual-luciferase reporter gene assay. Cell proliferation was detected by the CCK-8 method. Gene and protein expression levels were detected by reverse transcription quantitative PCR (RT-qPCR) and Western blotting. The TPC-1 cells were subcutaneously injected into the right posterior axillary region of nude mice to establish a xenograft tumor model of thyroid carcinoma, and the growth status of the tumors was recorded. Ki-67 and DDOST expression in xenograft tumor tissues was detected by immunohistochemistry. Lactate concentration and glucose consumption were measured using the corresponding assay kits. Results: Compared with normal thyroid cells Nthy-ori 3-1, the expression levels of miR-532-3p in thyroid cancer cell lines (TPC-1, FTC-133, IHH-4) were significantly decreased (P < 0.05), with the lowest level observed in TPC-1 cells. The expression of DDOST was significantly increased (P < 0.05). Overexpression of miR-532-3p inhibited TPC-1 cell proliferation and glycolysis and downregulated DDOST expression (P < 0.05). Moreover, these effects were reversed by DDOST overexpression (P < 0.05). Overexpression of miR-532-3p inhibited thyroid cancer xenograft growth and reduced DDOST expression in xenograft tumor tissues (P < 0.05). Conclusion: Overexpression of miR-532-3p inhibited TPC-1 cell proliferation and glycolysis by targeting DDOST and suppressed thyroid cancer xenograft growth in nude mice.
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