Chang Jian-Hua, Xu Bo-Wen, Shen Di, Zhao Wei, Wang Yue, Liu Jia-Liang, Meng Guang-Xiao, Li Guang-Zhen, Zhang Zong-Li
Department of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, No.107 Wenhua West Road, Lixia District, Jinan, 250012, Shandong, China.
Department of General Surgery, Gansu Province Hospital, Lanzhou, 730000, GanSu Province, China.
Cancer Cell Int. 2023 Mar 16;23(1):46. doi: 10.1186/s12935-023-02893-y.
Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Its invasiveness and ability to metastasize contributes to an extremely high patient mortality. However, the molecular mechanisms that underlie the characteristics of HCC progression are not well understood. BRF2 has been shown to be an oncogene in a number of tumors; however, its role in HCC has not yet been thoroughly examined. In this study, we identified and validated BRF2 as an oncogene in HCC, providing a new insight into HCC pathogenesis and therapeutic possibilities. We showed that BRF2 expression was significantly upregulated in HCC cell lines and tissues, while BRF2 depletion suppressed HCC metastasis and invasion. We then examined the upstream regulation of BRF2 and identified miR-409-3p as being predicted to bind to the 3' UTR of BRF2. We used a luciferase activity assay and functional verification to show that BRF2 is downregulated by miR-409-3p. Finally, we used bioinformatic analysis to show that BRF2 may be related to early HCC development through the Wnt/β-catenin signaling pathway.
肝细胞癌（HCC）是全球最常见的癌症之一。其侵袭性和转移能力导致患者死亡率极高。然而，HCC进展特征背后的分子机制尚未完全明确。BRF2已被证明在多种肿瘤中是一种癌基因；然而，其在HCC中的作用尚未得到充分研究。在本研究中，我们鉴定并验证了BRF2是HCC中的一种癌基因，为HCC发病机制和治疗可能性提供了新的见解。我们发现BRF2在HCC细胞系和组织中表达显著上调，而BRF2缺失则抑制了HCC的转移和侵袭。然后，我们研究了BRF2的上游调控，并确定miR-409-3p可预测与BRF2的3'UTR结合。我们通过荧光素酶活性测定和功能验证表明BRF2受miR-409-3p下调。最后，我们通过生物信息学分析表明BRF2可能通过Wnt/β-连环蛋白信号通路与早期HCC发展相关。
