Xie Lian, Xu Fangyin, Shi Ruixin, Zhang Zhendong, Pan Chenwei, Chen Ping
Wenzhou Medical University, Wenzhou, China.
Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Sci Rep. 2025 Aug 31;15(1):32009. doi: 10.1038/s41598-025-16785-w.
To investigate the biological functions of TOP2A in HCC using bioinformatics and single-cell RNA sequencing (scRNA-seq) methods, and to explore the functional consequences of TOP2A in HepG2 and Huh-7 cells with TOP2A knockdown. This study aims to provide new theoretical insights and potential therapeutic targets for the early diagnosis and targeted treatment of HCC. Through the analysis of single-cell RNA sequencing data, the immunological significance of TOP2A and its relationship with the diagnosis and prognosis of HCC were studied. The expression levels of TOP2A in HCC and normal liver epithelial cells were validated using quantitative PCR (QPCR). siRNA technology was employed to interfere with TOP2A expression in HepG2 and Huh7 cells, and a TOP2A knockdown cell line was established. The transfection efficiency of siRNA was measured using QPCR and Western Blotting. The impact of TOP2A knockdown on the proliferation of HCC cells was assessed using the CCK8 assay. The effect of TOP2A on the migration ability of HCC cells was observed through a wound-healing assay. The influence of TOP2A knockdown on the invasive ability of HCC cells was examined using the Transwell assay. The effect of TOP2A knockdown on the apoptosis of HCC cells was evaluated using flow cytometry. This study integrated single-cell RNA sequencing and functional analyses identified TOP2A as a critical oncogenic driver in HCC. TOP2A expression was significantly upregulated in HCC tissues and strongly correlated with poor patient prognosis (P < 0.05). In vitro experiments showed that the efficiency of TOP2A knockdown mediated by siRNA was over 70% (P < 0.05), and it significantly inhibited the proliferation, invasion and migration of HCC cells (P < 0.05), promoted cell apoptosis (P < 0.05). Mechanistically, scRNA-seq revealed that TOP2A may promotes Tmem-to-Tex differentiation through the SPP1-CD44 axis. These findings position TOP2A as both a prognostic biomarker and a potential therapeutic target for overcoming immune evasion in HCC. TOP2A is significantly upregulated in HCC, and its expression level can serve as an independent prognostic biomarker. Knockdown of TOP2A can significantly inhibit the malignant phenotype of HepG2 and Huh7 cells. Moreover, the analysis shows that TOP2A may promote immune escape by modulating the SPP1-CD44 axis and remodeling the immune microenvironment. These findings not only reveal the crucial role of TOP2A in the progression of HCC, but also indicate that it may become a potential target for immunotherapy in HCC, providing a new theoretical basis for improving the precise treatment strategies for HCC patients.
利用生物信息学和单细胞RNA测序(scRNA-seq)方法研究TOP2A在肝癌中的生物学功能,并探讨TOP2A基因敲低对HepG2和Huh-7细胞功能的影响。本研究旨在为肝癌的早期诊断和靶向治疗提供新的理论见解和潜在治疗靶点。通过分析单细胞RNA测序数据,研究TOP2A的免疫学意义及其与肝癌诊断和预后的关系。采用定量PCR(QPCR)验证TOP2A在肝癌和正常肝上皮细胞中的表达水平。运用siRNA技术干扰HepG2和Huh7细胞中TOP2A的表达,建立TOP2A基因敲低细胞系。使用QPCR和蛋白质免疫印迹法检测siRNA的转染效率。采用CCK8法评估TOP2A基因敲低对肝癌细胞增殖的影响。通过划痕愈合实验观察TOP2A对肝癌细胞迁移能力的影响。采用Transwell实验检测TOP2A基因敲低对肝癌细胞侵袭能力的影响。运用流式细胞术评估TOP2A基因敲低对肝癌细胞凋亡的影响。本研究整合单细胞RNA测序和功能分析,确定TOP2A是肝癌中关键的致癌驱动因素。TOP2A在肝癌组织中显著上调,与患者预后不良密切相关(P < 0.05)。体外实验表明,siRNA介导的TOP2A基因敲低效率超过70%(P < 0.05),并显著抑制肝癌细胞的增殖、侵袭和迁移(P < 0.05),促进细胞凋亡(P < 0.05)。机制上,scRNA-seq显示TOP2A可能通过SPP1-CD44轴促进Tmem向Tex分化。这些发现表明TOP2A既是一种预后生物标志物,也是克服肝癌免疫逃逸的潜在治疗靶点。TOP2A在肝癌中显著上调,其表达水平可作为独立的预后生物标志物。敲低TOP2A可显著抑制HepG2和Huh7细胞的恶性表型。此外,分析表明TOP2A可能通过调节SPP1-CD44轴和重塑免疫微环境促进免疫逃逸。这些发现不仅揭示了TOP2A在肝癌进展中的关键作用,还表明它可能成为肝癌免疫治疗的潜在靶点,为改进肝癌患者的精准治疗策略提供了新的理论依据。