CLDN1 and colon adenocarcinoma: This observation was accompanied by higher circulating levels of tumor necrosis α (TNF-α) and interferon γ (INF-γ), which have independently been shown to increase occludins and the internalization of claudin-1 and -4 and to downregulate expression of claudin-1, causing increased permeability in colonic adenocarcinoma-derived T84 epithelial cell lines [93].