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. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: Hum Cell. 2019 Mar 14;32(3):240–250. doi: 10.1007/s13577-019-00247-3

Figure 3: SLFN12 modulates butyrate-induced sucrase-isomaltase promoter activity in human intestinal epithelial Caco-2 cells.

Figure 3:

Caco-2 cells were transfected with empty vector or SI-promoter GoClone construct for 48 hours followed by treatment with PBS control (Cont) or 2mM butyrate (NaB) for additional 24hr. For siRNA studies, Caco-2 cells were co-transfected with SI-promoter construct and control siNT1 or SLFN12 siRNA (siSLFN12) for 48hours followed by treatment with 2mM butyrate for additional 24 hours, then luciferase activity was measured. (A) Basal SI-promoter activity increased in comparison to empty vector (n=5, *p<0.05) and NaB further increased SI-promoter activity in comparison to empty vector or SI-promoter construct alone (n=5, *p<0.05 vs empty vector; n=5, **p<0.05 vs SI-promoter alone). (B) SI-promoter activity after mechanical stimulation increased compared to control (static) cells (n=7, *p<0.05). (C) Knockdown efficiency of each of the siRNA putatively targeting SLFN12 (siRNA-1, siRNA-2, siRNA-3 and siRNA-4) with respect to control non-targeting siRNA (siNT-1) transfected in Caco-2 cells. Each siRNA was used at 100 nM (n = 4, *, p < 0.05, siNT vs siSLFN12). (D) Sodium butyrate enhances SI promoter activity in siNT1-treated cells (n = 5, *, p < 0.05). Reduced SLFN12 expression by siSLFN12 attenuated basal (n = 5, *, p < 0.05) and butyrate-induced SI-promoter activity (n=5, #, p<0.05).