目的：本研究旨在探讨miR-532-3p对甲状腺癌TPC-1细胞增殖及糖酵解的调控作用，并以多萜醇二磷酸寡糖蛋白糖基转移酶非催化亚基（DDOST）为靶标初步探讨其潜在机制。方法：检测正常甲状腺细胞Nthy-ori 3-1及甲状腺癌细胞TPC-1、FTC-133、IHH-4中miR-532-3p基础表达；根据检测结果选择TPC-1细胞进行后续实验，并将其分为mimic-NC组、miR-532-3pmimic组、inhibitor-NC组、miR-532-3p inhibitor组、mimic-NC + pcDNA-NC组、mimic-NC + pcDNA-DDOST组、miR-532-3p mimic+ pcDNA-NC组、miR-532-3p mimic + pcDNA-DDOST组。采用双萤光素酶报告基因实验检测miR-532-3p与DDOST的靶向关系。采用CCK-8法检测细胞增殖活力。采用实时荧光定量PCR（RT-qPCR）和蛋白质印迹（Western blotting）法检测mRNA和蛋白表达。将TPC-1细胞经皮下注射接种于裸小鼠右后侧腋窝处，构建甲状腺癌裸小鼠移植瘤模型，记录肿瘤生长情况。采用免疫组织化学法检测移植瘤组织中Ki-67和DDOST的阳性表达。采用乳酸检测试剂盒和葡萄糖检测试剂盒检测乳酸生成量及葡萄糖消耗率。结果：与正常甲状腺细胞Nthy-ori 3-1相比，甲状腺癌细胞（TPC-1、FTC-133、IHH-4）中miR-532-3p表达水平均明显降低（P < 0.05），其中TPC-1细胞中miR-532-3p表达水平最低，而DDOST的表达显著升高（P < 0.05）。过表达miR-532-3p可抑制TPC-1细胞增殖活力和糖酵解水平，并下调DDOST表达（P < 0.05），且这些作用可被DDOST过表达所逆转（P < 0.05）。过表达miR-532-3p可抑制裸小鼠甲状腺癌移植瘤生长，并降低移植瘤组织中DDOST的表达（P < 0.05）。结论：过表达miR-532-3p可通过靶向调控DDOST抑制TPC-1细胞增殖和糖酵解，进而抑制裸小鼠甲状腺癌移植瘤生长。

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.