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

• Published in: Cancers 2024-02, Vol.16 (4), p.752
• Main Authors: Zhu, Xiang, Zhang, Yong, Bian, Rui, Zhu, Jiyue, Shi, Weibin, Ye, Yuanyuan
• Format: Article
• Language: English
• Subjects: 1-Phosphatidylinositol 3-kinase; Actin; AKT protein; Antibodies; Apoptosis; Bioinformatics; Biotechnology; Cancer therapies; Carbon dioxide; Cell activation; Cell culture; Cell cycle; Cell growth; Cell migration; Cell proliferation; Chemotherapy; Efficiency; Experiments; Gallbladder cancer; Immunohistochemistry; Kinases; Medical research; Metastasis; Molecular modelling; Polymerase chain reaction; Protein-serine/threonine kinase; Proteins; Radiation therapy; Reagents; Signal transduction; Tumors; Western blotting
• ISSN: 2072-6694; 2072-6694
• DOI: 10.3390/cancers16040752

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