文章：

BAIAP2L2通过GABPB1介导的活性氧失衡促进肝细胞癌的恶性进展

BAIAP2L2 promotes the malignancy of hepatocellular carcinoma via GABPB1-mediated reactive oxygen species imbalance 

原文发布日期：2024-11-04 

英文摘要：

Hepatocellular carcinoma (HCC) is a common type of cancer worldwide and ranks as the fourth leading cause of cancer-related deaths. This research investigation identified an upregulation of BAI1-associated protein 2-like 2 (BAIAP2L2) in HCC tissues, which was found to be an independent prognostic factor for overall survival in HCC patients. BAIAP2L2 was observed to enhance cell proliferation, metastasis, stemness, cell cycle progression, and inhibit apoptosis in HCC. Mechanistically, NFκB1 was found to stimulate BAIAP2L2 transcription by directly binding to its promoter region. BAIAP2L2 interacts with GABPB1 to inhibit its ubiquitin-mediated degradation and promote its nuclear translocation. BAIAP2L2 inhibits the levels of reactive oxygen species (ROS) by regulating GABPB1, thereby promoting cancer properties in HCC and reducing the sensitivity of HCC to lenvatinib. In summary, this study elucidates the role and underlying mechanism of BAIAP2L2 in HCC, providing a potential biomarker and therapeutic target for this disease. 

摘要翻译：

肝细胞癌（HCC）是全球常见癌症类型，在癌症相关死亡中位列第四大病因。本研究发现肝细胞癌组织中BAI1关联蛋白2样蛋白2（BAIAP2L2）表达上调，该分子被证实是HCC患者总生存期的独立预后因素。研究观察到BAIAP2L2能增强HCC的细胞增殖、转移、干性特征和细胞周期进程，并抑制细胞凋亡。机制研究表明，NFκB1通过直接结合BAIAP2L2启动子区域激活其转录。BAIAP2L2与GABPB1相互作用，抑制其泛素介导的降解并促进其核转位。BAIAP2L2通过调控GABPB1降低活性氧（ROS）水平，从而促进HCC的恶性特性并降低肝癌对乐伐替尼的敏感性。综上所述，本研究阐明了BAIAP2L2在HCC中的作用及其潜在机制，为该疾病提供了潜在的生物标志物和治疗靶点。

原文链接：

BAIAP2L2 promotes the malignancy of hepatocellular carcinoma via GABPB1-mediated reactive oxygen species imbalance