目的：以生物信息学研究为基础，探讨miR-4674表达变化对BGC-823胃癌细胞系生物学特征的影响。方法：通过生物信息学分析，得到与胃癌关系密切的研究靶点miR-4674，构建miR-4674模拟物（mimic）、抑制物（inhibitor）以及相关阴性对照（NC）转染至BGC-823细胞系。应用逆转录聚合酶链式反应（RT-PCR）方法检测BGC-823细胞中miR-4674的表达变化。应用噻唑蓝（MTT）法检测细胞增殖能力。应用Transwell培养体系检测细胞迁移能力，应用TUNEL检测细胞的凋亡情况。结果：与空白对照组以及转染NC的细胞比较，转染miR-4674 mimic的细胞中miR-4674表达水平明显升高，细胞的增殖与迁移能力均明显升高（P<0.05），而转染miR-4674 inhibitor的细胞中miR-4674表达水平明显降低，细胞的增殖与迁移能力均明显下降（P<0.05）。TUNEL检测结果显示，各组均未见到凋亡细胞。结论：在BGC-823胃癌细胞系抑制miR-4674表达降低其恶性程度，在BGC-823胃癌细胞系过表达miR-4674则促进其恶性程度,miR-4674可能是胃癌干预的治疗靶点，为胃癌的治疗提供了新的策略。

Objective To explore the impact of miR-4674 expression changes on the biological characteristics of BGC-823 gastric cancer cell line based on bioinformatics research. Methods Through bioinformatics screening, miR-4674 was prioritized as a gastric cancer-associated miRNA. We constructed miR-4674 mimic, inhibitor, and corresponding negative control (NC) transfected into the BGC-823 cell line. Reverse transcription-polymerase chain reaction (RT-PCR) method was used to detect the expression changes of miR-4674 in BGC-823 cells. Functional assays included: MTT assay for cell proliferation ability; Transwell assay for migration capacity; TUNEL staining for cell apoptosis detection.Results Compared with the control group and cells transfected with NC, the level of miR-4674 was significantly increased in cells transfected with miR-4674 mimic, and the proliferation and migration abilities of the cells were significantly improved (P< 0.05). In cells transfected with miR-4674 inhibitor, the level of miR-4674 was significantly decreased, and the proliferation and migration abilities of the cells were significantly reduced (P<0.05). The result of TUNEL showed no significant differences in apoptotic rates were observed across all groups. Conclusions In the BGC-823 gastric cancer cell line, inhibition of miR-4674 expression can reduce its malignancy, while overexpression of miR-4674 can enhance its malignancy, suggesting its potential as a therapeutic target for gastric cancer intervention, providing a new strategy for the treatment of gastric cancer.