Department of Ophthalmology, The Affiliated Hospital of Qingdao University, 266003, Qingdao, China.
Tumor Immunology and Cytotherapy of Medical Research Center and Key Laboratory of Pancreatic Disease Clinical Research (Shandong Province), The Affiliated Hospital of Qingdao University, Qingdao 266000, China.
Cytokine. 2024 Dec;184:156771. doi: 10.1016/j.cyto.2024.156771. Epub 2024 Sep 27.
The impact of Ang-1 on tumors remains a subject of contention, with its mechanism of action exhibiting complexity in the progression of diverse tumor types. Ang-1 has been shown to promote the progression of glioma, glioma, esophageal and human cervical cancer, whereas it exerts inhibitory effects on the growth of breast and colon cancer. However, the specific function of Ang-1 in CM has not been clarified. This research aims to explore the function of Ang-1 on CM and the underlying mechanism. WB and qPCR were utilized to measure the expression levels of different factors in CM cells. Clonogenic, CCK-8 and Transwell migration assay were used to probe CM cells' proliferation and migration ability. Xenograft tumor model was used to testify the effect of Ang-1 and Artesunate (ART) on the growth of CM in vivo. We found Ang-1 promoted CM proliferation and migration, while it was inhibited by ART in vitro. Moreover, both ART treatment and Ang-1 knockdown had the effect of suppressing tumor growth in CM xenograft model. Mechanically, Ang-1 activated Akt/mTOR pathway and induced epithelial-mesenchymal transition (EMT) in CM cells. Furthermore, ART regulated Akt/mTOR pathway by decreasing the expression of Ang-1 in CM cells. Ang-1 promotes tumorigenesis of CM by regulating Akt/mTOR pathway, which can be inhibited by ART.
血管生成素 1(Ang-1)对肿瘤的影响仍然存在争议,其作用机制在不同类型肿瘤的进展中表现出复杂性。Ang-1 已被证明可促进神经胶质瘤、食管癌和宫颈癌的进展,而对乳腺癌和结肠癌的生长则具有抑制作用。然而,Ang-1 在 CM 中的具体功能尚未阐明。本研究旨在探讨 Ang-1 对 CM 的作用及其潜在机制。通过 WB 和 qPCR 测量 CM 细胞中不同因子的表达水平。集落形成、CCK-8 和 Transwell 迁移实验用于探测 CM 细胞的增殖和迁移能力。异种移植肿瘤模型用于体内验证 Ang-1 和青蒿琥酯(ART)对 CM 生长的影响。我们发现 Ang-1 促进 CM 的增殖和迁移,而 ART 在体外抑制其作用。此外,ART 治疗和 Ang-1 敲低均能抑制 CM 异种移植模型中的肿瘤生长。在机制上,Ang-1 通过激活 Akt/mTOR 通路诱导 CM 细胞发生上皮间质转化(EMT)。此外,ART 通过降低 CM 细胞中 Ang-1 的表达来调节 Akt/mTOR 通路。Ang-1 通过调节 Akt/mTOR 通路促进 CM 的肿瘤发生,而 ART 可以抑制该通路。