PDF(Pubmed)
Abstract：
The ANLN gene encodes anillin, a protein that binds to actin. Recent research has identified ANLN\'s function in the initiation and advancement of different cancers. However, its impact on gallbladder cancer (GBC) remains unexplored. This study aimed to elucidate its possible molecular mechanisms in GBC. ANLN expression was assessed using quantitative real-time polymerase chain reaction (QRT-PCR), Western blotting (WB), and immunohistochemistry (IHC), revealing elevated levels in GBC tissues. ANLN knockdown resulted in the inhibition of cell proliferation and migration, leading to apoptosis and cell cycle arrest. Conversely, ANLN overexpression had the opposite effects on GBC cells. In vivo experiments confirmed that ANLN knockdown inhibited GBC cell growth. RNA-seq and bioinformatics analysis revealed ANLN\'s function in activating the PI3K/AKT signaling pathway. We further confirmed that ANLN could upregulate STRA6 expression, which activated PI3K/AKT signaling to enhance the growth and movement of GBC cells. These findings demonstrate ANLN\'s involvement in GBC initiation and progression, suggesting its potential as a novel target for GBC.
摘要：
ANLN基因编码Anillin,与肌动蛋白结合的蛋白质。最近的研究已经确定了ANLN在不同癌症的发生和发展中的功能。然而,其对胆囊癌（GBC）的影响仍有待探索。本研究旨在阐明其在GBC中的可能分子机制。使用定量实时聚合酶链反应（QRT-PCR）评估ANLN表达，蛋白质印迹(WB),和免疫组织化学（IHC），显示GBC组织中水平升高。ANLN敲低导致细胞增殖和迁移的抑制，导致细胞凋亡和细胞周期停滞。相反，ANLN过表达对GBC细胞具有相反的作用。体内实验证实ANLN敲低抑制GBC细胞生长。RNA-seq和生物信息学分析揭示了ANLN在激活PI3K/AKT信号通路中的功能。我们进一步证实ANLN可以上调STRA6表达，激活PI3K/AKT信号以增强GBC细胞的生长和运动。这些发现表明ANLN参与GBC的启动和进展，表明其作为GBC新目标的潜力。
