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. 2014 Apr 2;9(4):e93651. doi: 10.1371/journal.pone.0093651

Figure 6. PL-induced survivin upregulation is dependent of EGFR, mTOR and MEK.

Figure 6

A–B: Islets were isolated from wild-type mice, stimulated with or without PL (500 ng/ml), gefitinib (2 μM), rapamycin (10 nM), MEK inhibitor PD0325901 (0,5 μM) or EGF (50 ng/ml) and BTC (50 ng/ml) for 96 h and RT-qPCR performed. Graph is showing the relative mRNA level of survivin (A) and Tph1 (B). n = 6–9 per group. Bars represent the mean ±SEM for each group. *p<0.05, **p<0.01 ***p<0.001. C: Proposed model for PL-induced survivin upregulation. Prl-R activation leads to transactivation of EGFR, which activates MAPK and PI3K-Akt-mTOR pathways, that together stimulate survivin gene expression.