Mannose-binding lectin 2 (MBL2), a member of the multimeric lectin family, is crucial in immune regulation and tumor development.MBL2gene polymorphisms are associated with the risk and prognosis of various tumors, including hepatocellular carcinoma (HCC). Its functional role in HCC remains largely unclear. In this study, we aimed to identify whetherMBL2is a key regulator and a potential therapeutic target for HCC. A bioinformatics analysis revealed close relationships amongMBL2downregulation, the tumor-associated proliferation and metastasis pathway, and tumor immunosuppressive microenvironments. Lower expression ofMBL2in HCC patients was linked to an unfavorable prognosis. A cell counting kit-8 assay, colony formation assay, transwell migration assay, and wound healing assay further confirmed that the overexpression ofMBL2could directly inhibit the proliferation and metastasis of HCC. Moreover,MBL2expression was regulated by miR-34c-3p, as confirmed by the dual-luciferase reporter assay, thereby demonstrating tumor progression in HCC cells. Thus, our study offers the first comprehensive confirmation of the role ofMBL2in the development of HCC through multi-omics analysis and experimental validation. Furthermore, miR-34c-3p was found to be an upstream mechanism of the downregulation ofMBL2expression and could be a promising therapeutic target, expanding treatment options for patients with HCC.
甘露糖结合凝集素2（MBL2）作为多聚凝集素家族成员，在免疫调节与肿瘤发生发展中具有关键作用。MBL2基因多态性与包括肝细胞癌（HCC）在内的多种肿瘤风险及预后密切相关，但其在HCC中的具体功能机制尚不明确。本研究旨在探究MBL2是否可作为HCC的关键调控因子及潜在治疗靶点。生物信息学分析显示，MBL2表达下调与肿瘤增殖转移通路及免疫抑制微环境存在密切关联。HCC患者中MBL2低表达与不良预后显著相关。通过CCK-8实验、克隆形成实验、Transwell迁移实验及划痕实验进一步证实，过表达MBL2可直接抑制HCC细胞的增殖与转移能力。双荧光素酶报告基因实验验证miR-34c-3p可调控MBL2表达，从而介导HCC细胞肿瘤进展。本研究首次通过多组学分析与实验验证，系统阐明了MBL2在HCC发展中的作用机制。此外，发现miR-34c-3p是MBL2表达下调的上游调控机制，可能成为极具前景的治疗靶点，为HCC患者拓展了治疗选择。
肿瘤(癌症)患者之家