NF-kappaB subtypes regulate CCCTC binding factor affecting corneal epithelial cell fate.

The Journal of Biological Chemistry
Luo LuJie Wang

Abstract

CCCTC binding factor (CTCF) controls DNA imprinting, insulates important gene expression, and mediates growth factor- and stress-induced cell fate. However, regulatory mechanisms involved in intracellular CTCF activity are largely unknown. In this study, we show that epidermal growth factor (EGF)-induced increase and UV stress-induced decrease in CTCF activities mediate human corneal epithelial cell proliferation and apoptosis, respectively. CTCF is regulated by activation of different NF-kappaB subtypes via stimulation by EGF and UV stress. EGF-induced formation of a p65/p50 heterodimer activated CTCF transcription to promote cellular proliferation. This was accomplished by the heterodimer binding to a kappaB site in the promoter region of CTCF gene. In contrast, UV stress induced formation of a p50/p50 homodimer, which suppressed CTCF expression leading to apoptosis. Thus, CTCF by itself plays a central role in mediating the dichotomous effects of growth factor- and stress-stimulated NF-kappaB activation on cell survival and death. These results suggest that CTCF is a downstream component of the NF-kappaB pathway involved in the core transcriptional network of cell fate.

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Citations

Dec 20, 2011·Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology·Zheng WangPeter S Reinach
Jul 18, 2020·Scientific Reports·Simon Menanteau-LedoubleMansour El-Matbouli
Jan 8, 2021·PLoS Genetics·Bettina J LehmanBeverly M Emerson

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