文章：

ANLN通过STRA6介导的PI3K/AKT信号通路激活促进胆囊癌细胞的增殖与迁移

ANLNPromotes the Proliferation and Migration of Gallbladder Cancer Cells via STRA6-Mediated Activation of PI3K/AKT Signaling

原文发布日期：11 February 2024

DOI: 10.3390/cancers16040752

类型: Article

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英文摘要：

TheANLNgene encodes anillin, a protein that binds to actin. Recent research has identifiedANLN’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.ANLNexpression was assessed using quantitative real-time polymerase chain reaction (QRT-PCR), Western blotting (WB), and immunohistochemistry (IHC), revealing elevated levels in GBC tissues.ANLNknockdown resulted in the inhibition of cell proliferation and migration, leading to apoptosis and cell cycle arrest. Conversely,ANLNoverexpression had the opposite effects on GBC cells. In vivo experiments confirmed thatANLNknockdown inhibited GBC cell growth. RNA-seq and bioinformatics analysis revealedANLN’s function in activating the PI3K/AKT signaling pathway. We further confirmed thatANLNcould upregulate STRA6 expression, which activated PI3K/AKT signaling to enhance the growth and movement of GBC cells. These findings demonstrateANLN’s involvement in GBC initiation and progression, suggesting its potential as a novel target for GBC.

摘要翻译： 

ANLN基因编码的蛋白为anillin，是一种能够与肌动蛋白结合的蛋白质。近期研究已明确ANLN在不同癌症的发生与发展中具有重要作用，但其在胆囊癌中的具体影响尚未明确。本研究旨在阐明ANLN在胆囊癌中可能发挥的分子机制。通过实时定量聚合酶链反应、蛋白质印迹法和免疫组织化学技术检测发现，ANLN在胆囊癌组织中表达水平显著升高。敲低ANLN表达可抑制胆囊癌细胞增殖与迁移，并诱导细胞凋亡和细胞周期阻滞；而过表达ANLN则产生相反效应。体内实验进一步证实，敲低ANLN能够抑制胆囊癌细胞生长。RNA测序与生物信息学分析显示，ANLN通过激活PI3K/AKT信号通路发挥作用。我们进一步证实ANLN可上调STRA6表达，从而激活PI3K/AKT信号通路，促进胆囊癌细胞的生长与迁移。这些发现揭示了ANLN在胆囊癌发生发展中的关键作用，提示其可能成为胆囊癌治疗的新靶点。

原文链接：

ANLNPromotes the Proliferation and Migration of Gallbladder Cancer Cells via STRA6-Mediated Activation of PI3K/AKT Signaling