Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. Johns University, 8000 Utopia Parkway, Jamaica, NY 11439, USA.
Mediators Inflamm. 2017;2017:6589423. doi: 10.1155/2017/6589423. Epub 2017 Sep 24.
Chronic inflammation is associated with cancer. CXCL8 promotes tumor microenvironment construction through recruiting leukocytes and endothelial progenitor cells that are involved in angiogenesis. It also enhances tumor cell proliferation and migration. Metformin, type II diabetes medication, demonstrates anticancer properties via suppressing inflammation, tumor cell proliferation, angiogenesis, and metastasis. This study intended to address the role of metformin in regulation of CXCL8 expression and cell proliferation and migration. Our data indicated that metformin suppressed LPS-induced CXCL8 expression in a dose-dependent manner through inhibiting NF-B, but not AP-1 and C/EBP, activities under the conditions we used. This inhibitory effect of metformin is achieved through dampening LPS-induced NF-B nuclear translocation. Cell migration was inhibited by metformin under high dose (10 mM), but not cell proliferation.
慢性炎症与癌症有关。CXCL8 通过招募参与血管生成的白细胞和内皮祖细胞来促进肿瘤微环境的构建。它还增强了肿瘤细胞的增殖和迁移。二甲双胍是一种治疗 2 型糖尿病的药物，通过抑制炎症、肿瘤细胞增殖、血管生成和转移来发挥抗癌作用。本研究旨在探讨二甲双胍在调节 CXCL8 表达和细胞增殖及迁移中的作用。我们的数据表明，二甲双胍通过抑制 NF-κB 而不是 AP-1 和 C/EBP 的活性，以剂量依赖的方式抑制 LPS 诱导的 CXCL8 表达，在我们使用的条件下。二甲双胍的这种抑制作用是通过抑制 LPS 诱导的 NF-κB 核转位来实现的。高剂量（10mM）的二甲双胍抑制细胞迁移，但不抑制细胞增殖。
