目的：探究miR-218-5p靶向磷酸二酯酶7A（PDE7A）调节人非小细胞肺癌（NSCLC）A549细胞糖酵解过程的机制。方法：常规培养A549细胞，用Lipo3000将miR-218-5p mimic、mimic-NC、PDE7A过表达质粒（PDE7A-oe）和PDE7A对照质粒（PDE7ANC）转染A549细胞，记为miR-218-5p mimic组、mimic-NC组、PDE7A-oe组和PDE7A-NC组。qPCR法验证转染效率，WB法检测糖酵解关键酶蛋白的表达，葡萄糖测定法和乳酸生成测定法检测各转染组A549细胞中2脱氧葡萄糖和乳酸含量，双萤光素酶报告基因实验验证miR-218-5p与PDE7A靶向结合关系，用TCGA数据库数据分析PDE7A mRNA在肺癌组织中的表达水平。结果：在A549细胞中成功地过表达了miR-218-5p（P<0.01）。过表达miR-218-5p均能显著抑制A549细胞中PDE7A、HK2、PKM2蛋白的表达（均P<0.01）、葡萄糖摄取量和乳酸生成量（均P<0.01）。过表达PDE7A均可显著促进A549细胞中PDE7A、HK2、PKM2蛋白的表达（均P<0.01），以及葡萄糖摄取量和乳酸生成量（均P<0.01）。A549细胞中miR-218-5p可与PDE7A mRNA的3′-UTR直接结合。数据库数据分析结果显示，PDE7A mRNA在肺鳞状细胞癌组织中呈高表达（P<0.01）。结论： miR-218-5p靶向PDE7A调控A549细胞中HK2和PKM2的表达水平，进而抑制糖酵解过程，miR-218-5p/PDE7A可能是NSCLC临床诊断和治疗的潜在靶点。

Objective: To investigate the mechanism of miR-218-5p regulating the glycolytic process in human non-small cell lung cancer A549 cells by targeting phosphodiesterase 7A (PDE7A). Methods: A549 cells were routinely cultured, and miR-218-5p mimic, mimic-NC, PDE7A overexpression plasmid (PDE7A-oe) and PDE7A control plasmid (PDE7A-NC) were transfected into A549 cells using Lipo3000, and recorded as the miR-218-5p mimic group, the mimic-NC group, the PDE7A-oe group and the PDE7A-NC group. The transfection efficiency was verified by qPCR assay; the expressions of glycolysis key enzyme proteins were detected by WB assay; the 2-deoxyglucose and lactate contents in A549 cells of each transfection group were detected by glucose assay and lactate production assay; the target binding relationship between miR-218-5p and PDE7A was verified by dual-luciferase reporter gene assay, and the data from the TCGA database were used to analyze the expression level of PDE7A mRNA in lung cancer tissues. Results: miR-218-5p was successfully overexpressed in A549 cells (P<0.01). Overexpression of miR-218-5p significantly inhibited the expressions of PDE7A, HK2, PKM2 proteins (all P<0.01), glucose uptake and lactate production (both P<0.01) in A549 cells. Overexpression of PDE7A significantly promoted the expressions of PDE7A, HK2, and PKM2 proteins (all P<0.01), as well as glucose uptake and lactate production (both P<0.01) in A549 cells. miR-218-5p in A549 cells could directly bind to the 3′-UTR of PDE7A mRNA. Database data analysis showed that PDE7A mRNA was highly expressed in lung squamous cell carcinoma tissues (P<0.01). Conclusion: miR-218-5p targets PDE7A to regulate the expression levels of HK2 and PKM2 in A549 cells, which in turn inhibits the glycolytic process. miR-218-5p/PDE7A may be a potential target for clinical diagnosis and treatment of NSCLC.

内蒙古自治区卫生健康科技计划项目（No.202202242）和内蒙古医学科学院公立医院科研联合基金科技项目（No.2023GLLH0206）