The Involvement of NF-κB/Klotho Signaling in Colorectal Cancer Cell Survival and Invasion
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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.
KeywordsLPS NF-κB Colorectal cancer Klotho
This study was supported by the Postdoctoral Science Foundation of China (2016 M602416), National Natural Science Foundation of China (81704089), Postdoctoral Science Fund Special Grant of China (2017 T100603), 2016 Postdoctoral Researcher Daily Funding of Hunan Province (49), the Department of Education Key Project of Hunan Province (15A024), and Changsha City’s Outstanding Innovation Youth Training Program (kq 1707012).
Compliance with Ethical Standards
Conflict of Interest
All authors declared no conflict of interest.
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