摘要： 目的 探讨锌指蛋白502 （ZNF502）在肺腺癌中的表达情况、临床意义及分子机制。方法 通过肿瘤基因组图谱（TCGA）分析ZNF502在肺腺癌中的mRNA表达，以及与生存危险因素的相关性。采用Kaplan-Meier法分析ZNF502与患者预后的关系。通过linkedomics网站对ZNF502的下游差异基因进行基因集富集分析（GSEA），并采用Western blotting对下游关键分子进行验证。运用免疫荧光实验确定ZNF502蛋白在肺腺癌细胞株的定位。MTS细胞增殖实验、克隆形成实验和EdU实验检测ZNF502过表达对肿瘤细胞增殖能力的影响。结果 ZNF502在肺腺癌组织中呈显著低表达（P < 0.05），主要定位于细胞核，且与肺腺癌患者的良好预后呈正相关。富集分析结果显示，ZNF502负调控细胞增殖和G₂/M检查点相关通路，导致细胞周期阻滞。ZNF502过表达显著抑制肺腺癌细胞增殖能力，并下调G₂/M检查点关键蛋白的表达。结论 ZNF502在肺腺癌中低表达，其通过调控细胞周期抑制肺腺癌细胞的增殖，延缓肿瘤发生发展。

锌指蛋白502在肺腺癌中的表达及作用机制

马小雯^1,2, 范明伟¹, 杜江¹

中国医科大学 1. 基础医学院病理学教研室;
2. 临床二系106期, 沈阳 110122

收稿日期:2023-03-02出版日期:2023-09-30发布日期:2023-09-02
通讯作者:杜江E-mail:cmuduj@163.com
作者简介:马小雯(2002-),女,本科在读.
基金资助:辽宁省自然科学基金（2020-BS-098）；2023年中国医科大学大学生创新创业训练计划


关键词: 肺腺癌, 锌指蛋白502, 细胞增殖
Abstract: Objective To investigate the expression of zinc finger protein 502 (ZNF502) in lung adenocarcinoma and its clinical signifi-cance and molecular mechanism. Methods The mRNA expression of ZNF502 in lung adenocarcinoma and its correlation with survival risk factors were analyzed by the TCGA database. Kaplan-Meier method was used to analyze the relationship between ZNF502 and the prognosis of the patients. The downstream differential genes of ZNF502 were subjected to GSEA enrichment analysis by the Linkedomics website, and the downstream key molecules were detected by Western blotting. The localization of the ZNF502 protein in the lung adenocarcinoma cell line was determined by immunofluorescence assay. MTS, colony formation assay, and EdU assay were used to detect the effect of ZNF502 overexpression on the proliferation of tumor cells. Results The expression of ZNF502 was significantly lower in lung adenocarcinoma (P < 0.05). ZNF502 was mainly localized in the nucleus and positively correlated with the good prognosis of lung adenocarcinoma. Furthermore, enrichment analysis showed that ZNF502 negatively regulated cell proliferation and G₂/M checkpoint-related pathways, resulting in cell cycle arrest. Overexpression of ZNF502 significantly inhibited the proliferation of lung adenocarcinoma cells and down-regulated the expression of key proteins at the G₂/M checkpoint. Conclusion The expression of ZNF502 was low in lung adenocarcinoma. ZNF502 inhibited the proliferation of lung adenocarcinoma cells by regulating the cell cycle, then decreased tumor development.
Key words: lung adenocarcinoma, zinc finger protein 502, cell proliferation
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