Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong University, Jiangsu 226001, China.
Department of Pathophysiology, School of Medicine, Nantong University, Jiangsu 226001, China.
Biomed Res Int. 2021 Mar 17;2021:6697476. doi: 10.1155/2021/6697476. eCollection 2021.
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide, and angiogenesis has been proven to be significantly involved in its progression. However, the molecular mechanism underlying HCC angiogenesis has not been well researched. In this study, RNA Binding Motif Protein 23 (RBM23) was identified as a novel proangiogenic factor in HCC cell lines and tissues.
Firstly, we analyzed the correlation of clinical specimens. In HCC tissues, the levels of RBM23 and microvessel density (MVD) showed a strong positive correlation. Furthermore, data from related cytology experiments showed that the knockdown of RBM23 expression in HCC cells significantly inhibited the tube formation by the human vascular endothelial cells in vitro. The mechanism of this phenomenon was found to be through increasing the mRNA of p65 and enhanced the nuclear accumulation of p65. Consequently, RBM23 activated the NF-B signaling pathway and promoted expression of the proangiogenic cytokines selectively. . In summary, this study revealed that RBM23 promotes the angiogenesis properties of HCC via the NF-B signaling pathway. It may, therefore, be a potential therapeutic target for the treatment of hepatocellular carcinoma.
肝细胞癌（HCC）是全球癌症相关死亡的主要原因，已有研究证实血管生成在其进展中起着重要作用。然而，HCC 血管生成的分子机制尚未得到很好的研究。在本研究中，RNA 结合基序蛋白 23（RBM23）被鉴定为 HCC 细胞系和组织中的一种新型促血管生成因子。
首先，我们分析了临床标本的相关性。在 HCC 组织中，RBM23 的水平与微血管密度（MVD）呈强烈正相关。此外，相关细胞学实验数据表明，在 HCC 细胞中敲低 RBM23 的表达，可显著抑制人血管内皮细胞的体外管形成。发现这一现象的机制是通过增加 p65 的 mRNA，并增强 p65 的核积累。因此，RBM23 激活了 NF-B 信号通路，并选择性地促进了促血管生成细胞因子的表达。综上所述，本研究揭示了 RBM23 通过 NF-B 信号通路促进 HCC 的血管生成特性。因此，它可能成为治疗肝细胞癌的潜在治疗靶点。
