The Involvement of NF-kappa B/Klotho Signaling in Colorectal Cancer Cell Survival and Invasion
The Involvement of NF-kappa B/Klotho Signaling in Colorectal Cancer Cell Survival and Invasion
复制标题
NF-kappa B/Klotho 信号转导在结直肠癌细胞存活和侵袭中的作用
DOI：
10.1007/s12253-018-0493-6
复制
发表时间：
2019
影响因子：
2.8
通讯作者：
He Yongheng
中科院分区：
文献类型：
--
作者：
Xie Biao;Nie Shaolin;Hu Gui;Xiong Li;Hu Fan;Li Mei;Peng Tianshu;Nie Jing;He Yongheng
脂多糖显著增加SW480和HT29结直肠癌细胞的侵袭力、细胞增殖和磷酸化的NF-IGFBp65和κ-1R蛋白，但降低Klotho蛋白的表达、细胞凋亡率和亚G0/G1期细胞百分率。相反，核因子-κB抑制剂表现出内毒素的拮抗作用。Toll样受体4shRNA可显著降低Klotho蛋白表达、细胞凋亡率和亚G0/G1期细胞百分率，显著降低磷酸化NF-IGFBp65和磷酸化κ-1R蛋白水平，降低侵袭力。综上所述，炎症抑制因子通过激活Toll样受体4/NF-κB信号通路在结直肠癌细胞中表达。
Lipopolysaccharide significantly increased invasion, cell proliferation, and phospho-NF-κB p65 and phospho-IGF-1R protein, but decreased klotho protein expression, cell apoptosis, and the percentage of sub G0/G1 cells in SW480 and HT29 colorectal cancer cells. In contrast, NF-κB inhibitor exhibited a counteract effect of lipopolysaccharide. Transfection of Toll-like receptor 4 shRNA significantly decreased phospho-NF-κB p65 and phospho-IGF-1R protein levels, invasion, but significantly increased klotho protein expression, cell apoptosis, and the percentage of sub G0/G1 in SW480 and HT29 cells. In conclusion, inflammation inhibitsklothogene expression in colorectal cancer cells through activation of Toll-like receptor 4 /NF-κB signal pathway.