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Figure 6 | Molecular Cancer

Figure 6

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 6

Nicotine induces proliferation and invasion of pancreatic cancer cells. (A) Quiescent CD18 cells were stimulated with 1 μM nicotine for 18 h and S-phase entry was measured by BrdU assays. The proliferative effects of nicotine in pancreatic cancer cells were abrogated in the MUC4 silenced cells, indicating that MUC4 function is required for the proliferative effects of nicotine. (B) Shows the efficiency of MUC4-siRNA transfection in CD18 cells. (C) Quantification of proliferation assay. (D) Nicotine was able to potently promote invasion of CD18 cells at a concentration of 1 μM as seen in a Boyden-chamber assay. The pro-invasive activity of nicotine was abrogated by MUC4-siRNA demonstrating a requirement for MUC4 role in invasion. Graphical representation of the results from Boyden-chamber assay shows the results are significant (*p ≤ 0.01, **p ≤ 0.04). (E ) RA was able to potently promote invasion of CD18 cells at a concentration of 10 nM as seen in a Boyden-chamber assay. The pro-invasive activity of RA was abrogated by MUC4-siRNA significantly demonstrating a requirement for MUC4 role in invasion. Graphical representation of the results from Boyden-chamber assay (*p ≤ 0.01, **p ≤ 0.03).

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Molecular Cancer

ISSN: 1476-4598