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Figure 3 | Molecular Cancer

Figure 3

From: Nicotine, IFN-γ and retinoic acid mediated induction of MUC4 in pancreatic cancer requires E2F1 and STAT-1 transcription factors and utilize different signaling cascades

Figure 3

E2F1 and STAT1 are necessary for MUC4 induction by nicotine, IFNγ and RA. Real time-PCR showing the expression of MUC4 in CD18/HPAF, ASPC-1, CAPAN-2 and SW1990 pancreatic cancer cells where E2F1 and STAT1 are knocked down using respective siRNAs and subjected to nicotine stimulation (A). Real time-PCR showing the effect of siRNA targeting E2F1 or STAT1 on expression of Muc 4 in response to IFN-γ stimulation in CD18/HPAF pancreatic cancer cells (B). Real time-PCR showing the effect of siRNA targeting E2F1 or STAT1 on expression of Muc 4 in response to RA stimulation in CD18/HPAF pancreatic cancer cells (C). The efficiency of E2F1-siRNA and STAT1-siRNA transfection in CD18 cells is also shown by Real time-PCR (D). (E) Chip assay results suggest that α7-subunit of nAChR play an important role in mediating nicotine-induced up-regulation of MUC4 expression in CD18/ HPAF cells. (F) Real time-PCR showing the reduction in the expression of MUC4 in CD18/HPAF cells treated with α-BT prior to nicotine stimulation. Nicotine induces MUC4 in a receptor-dependent fashion (*p ≤ 0.01, **p ≤ 0.03).

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