A. Nuclear fraction obtained from 50 μM of DCA and CDCA treated CD18/HPAF cells, demonstrated increased levels of FXR compared to the untreated control. On the other hand, FXR expression was more on the cytoplasmic fraction in untreated cells than DCA and CDCA treated cells. B. FXR expression was found to be significantly high in PC cell lines than normal pancreatic cells (HDPE). C. FXR was transiently knockdown in CD18/HPAF and T3M4 cell lines using 150 nM of siRNA oligos and confirmed using immunoblotting. Interestingly, FXR knockdown cells exhibited significant decline in FAK, pFAK (Tyr397), src, p-src (Tyr416), c-Jun, p-c-Jun (Ser63) and MUC4, suggestive of FXR involvement as the most upstream molecule in this BA-mediated FAK/c-Jun/MUC4 axis. D. The graphical representation of the result obtained from real-time PCR showing that knockdown of FXR in CD18/HPAF cell line leads to significant attenuation of both DCA (25 μM) or CDCA (25 μM)-mediated MUC4 upregulation. (*p<0.05, **p<0.01, ns means non-significant)