Human macrophage inflammatory protein‐3α/CCL20/LARC/Exodus/SCYA20 is transcriptionally upregulated by tumor necrosis factor‐α via a non‐standard NF‐κB site

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Abstract
The 5′‐flanking sequences of the human macrophage inflammatory protein‐3α/CCL20 gene were cloned and transfected into G‐361 human melanoma cells in a luciferase reporter construct. Tumor necrosis factor‐α (TNF‐α) treatment stimulated luciferase expression, and promoter truncations demonstrated that TNF‐α inducibility is conferred by a region between nt −111 and −77, which contains a non‐standard nuclear factor‐κB (NF‐κB) binding site. The requirement for NF‐κB was demonstrated as follows: (i) mutations in this NF‐κB site abrogated TNF‐α responsiveness; (ii) TNF‐α activated a construct containing two copies of the CCL20 NF‐κB binding site; (iii) overexpression of NF‐κB p65 activated the CCL20 promoter; (iv) NF‐κB from nuclear extracts of TNF‐α‐stimulated cells bound specifically to this NF‐κB site.

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