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. 2015 Nov 25;146(2):236–242. doi: 10.3945/jn.115.216580

FIGURE 6.

FIGURE 6

Differential regulation of FXR expression by secondary bile DCA in wild-type APC and APC-deficient human colon cancer cells. (A) Bars represent qRT-PCR quantitation (fold of DMEM) from 2 separate experiments performed in triplicate of FXR corrected for GAPDH as internal control in human HCT-116 (wild-type APC) and HT-29 (inactivated APC) colon cancer cells after 72 h of treatment with 50 μM DCA. Values are means ± SEMs. *Different from DMEM, P < 0.05. (B) Methylated PCR products were amplified with human FXR-M and β-ACTIN methylation-specific primers using as a template bisulfonated genomic DNA obtained from HCT-116 and HT-29 colon cancer cells. (C) Bands are representative immunocomplexes detected by Western blotting for FXR and β-ACTIN in HCT-116 and HT-29 cells cultured in control DMEM or DMEM supplemented with DCA. APC, adenomatous polyposis coli; DCA, deoxycholic acid; FXR, farnesoid X receptor; FXR-M, FXRα3/4 promoter methylation.