Abstract：
Lectin galactoside-binding soluble 3-binding protein (LGALS3BP) is associated with cancer metastasis and is a promising prognostic marker in neoplasms. In hepatocellular carcinoma (HCC), the prognostic impact and pro-metastatic function of LGALS3BP remain unclear. This study evaluated the endogenous LGALS3BP expression in HCC tissue and its association with prognosis. LGALS3BP protein levels were significantly elevated in clinical HCC tissues and cell lines. Increased LGALS3BP expression was closely associated with disease progression in HCC patients, and they also exhibited an unfavorable prognosis. Furthermore, the knockdown of LGALS3BP inhibited the growth, migration, and invasion of HCC cells in vitro. In mice xenografts, silencing LGALS3BP significantly inhibited tumor cell growth in vivo. Mechanically, upon LGALS3BP depletion, the tumor-suppressive function was dependent on inactivating Phosphatidylinositol 3-kinase (PI3K)/V-akt murine thymoma viral oncogene homolog (AKT) signaling pathway. Collectively, these findings suggest that LGALS3BP employs a pro-tumorigenic function in HCC and may be a promising HCC prognostic marker.
摘要：
凝集素半乳糖苷结合可溶性3结合蛋白（LGALS3BP）与癌症转移有关，并且是肿瘤中有希望的预后标志物。在肝细胞癌（HCC）中，LGALS3BP的预后影响和前转移功能尚不清楚.本研究评估了内源性LGALS3BP在HCC组织中的表达及其与预后的关系。LGALS3BP蛋白水平在临床HCC组织和细胞系中显著升高。LGALS3BP表达的增加与HCC患者的疾病进展密切相关。他们也表现出不利的预后。此外，LGALS3BP的敲除抑制了生长，迁移,和肝癌细胞的体外侵袭。在小鼠异种移植物中，沉默LGALS3BP可显著抑制体内肿瘤细胞生长。机械上,在LGALS3BP耗尽后，肿瘤抑制功能依赖于磷脂酰肌醇3-激酶(PI3K)/V-akt鼠胸腺瘤病毒癌基因同源物(AKT)信号通路的失活.总的来说，这些发现表明LGALS3BP在HCC中具有促肿瘤功能,并且可能是一个有前景的HCC预后标志物.
