NF-κB/Klotho 信号通路在结直肠癌细胞存活和侵袭中的作用。
The Involvement of NF-κB/Klotho Signaling in Colorectal Cancer Cell Survival and Invasion.
机构信息
Department One of Anorectal Surgery, The Second Affiliated Hospital of Hunan University of Chinese Medicine, 139 Renmin Road, Changsha, Hunan, 410005, People's Republic of China.
Department of Colorectal Surgery, Hunan Province Tumor Hospital, Changsha, 410013, Hunan, China.
出版信息
Pathol Oncol Res. 2019 Oct;25(4):1553-1565. doi: 10.1007/s12253-018-0493-6. Epub 2019 Jan 5.
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 inhibits klotho gene expression in colorectal cancer cells through activation of Toll-like receptor 4 /NF-κB signal pathway.
脂多糖显著增加了 SW480 和 HT29 结肠癌细胞的侵袭、细胞增殖、磷酸化 NF-κB p65 和磷酸化 IGF-1R 蛋白的表达，而降低了 klotho 蛋白的表达、细胞凋亡以及 sub G0/G1 细胞的比例。相反，NF-κB 抑制剂表现出对脂多糖的拮抗作用。Toll 样受体 4 shRNA 的转染显著降低了 SW480 和 HT29 细胞中磷酸化 NF-κB p65 和磷酸化 IGF-1R 蛋白的水平、侵袭，但显著增加了 klotho 蛋白的表达、细胞凋亡以及 sub G0/G1 细胞的比例。总之，炎症通过激活 Toll 样受体 4/NF-κB 信号通路抑制了结肠癌细胞中 klotho 基因的表达。
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