肝细胞癌（HCC）是一种常见的恶性肿瘤，其特征是广泛的血管生成。然而，HCC发病机制的潜在机制仍不清楚。先前的研究表明，RNA 结合蛋白 (RBP) 与 HCC 发病机制有关。在本研究中，我们观察到HCC组织中RBM28表达增加与肿瘤微血管密度呈正相关，与患者预后呈负相关。 HCC细胞中RBM28的过度表达促进人脐静脉内皮细胞的小管形成，而RBM28的抑制则具有相反的作用，此外，使用转基因小鼠模型和化学诱导的HCC模型评估了RBM28在HCC进展中的作用。我们使用各种分子测定和高通量检测方法来评估 RBM28 在促进 HCC 血管生成中的作用。 HCC中RBM28表达增加，直接与STAT3 mRNA结合，招募EIF4E增加STAT3表达，增强血管内皮生长因子A的分泌和表达；因此，促进 HCC 的新血管形成。使用多队列临床样本和动物模型评估了 RBM28 作为 HCC 可行的诊断和治疗靶点的潜力。总之，我们的结果为 HCC 的发病机制、临床诊断和治疗提供了见解。版权所有 © 2024。由 Elsevier B.V. 出版。

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor characterized by extensive angiogenesis. However, the underlying mechanisms of HCC pathogenesis remain unclear. Previous studies have shown that RNA-binding proteins (RBPs) are implicated in HCC pathogenesis. In this study, we observed that increased RBM28 expression in HCC tissues was positively correlated with tumor microvascular density and negatively correlated with patient prognosis. Overexpression of RBM28 in HCC cells promoted tubule formation in human umbilical vein endothelial cells, whereas inhibition of RBM28 had the opposite effect, furthermore, the role of RBM28 in the progression of HCC was assessed using transgenic mouse models and chemically induced HCC models. We used various molecular assays and high-throughput detection methods to evaluate the role of RBM28 in promoting angiogenesis in HCC. Increased RBM28 expression in HCC directly binds to STAT3 mRNA, recruiting EIF4E to increase STAT3 expression and enhancing the secretion and expression of vascular endothelial growth factor A; consequently, promoting neovascularization in HCC. The potential of RBM28 as a viable diagnostic and therapeutic target for HCC was assessed using multi-cohort clinical samples and animal models. In summary, our results provide insights into the pathogenesis, clinical diagnosis, and treatment of HCC.Copyright © 2024. Published by Elsevier B.V.