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. 2015 Jun 12;5:10867. doi: 10.1038/srep10867

Figure 7. Knockdown of Caveolin-1 leads to decreased STAT3, Src and proliferative signaling in vitro.

Figure 7

(A) shCav-1 downregulated cells in both MIAPaCa-2 and BxPC3 cell lines showed decreased phosphoJAK2 at residues Tyr1007/1008 and phosphoSTAT3 at Tyr705 as compared to scrambled control shRNA cells. Total levels of JAK2 and STAT3 are unchanged. SOCS2 and PIAS3, both inhibitors of the JAK-STAT pathway, are upregulated in Cav-1 knockdown cells. Phosphorylation of Src at Tyr416, the activation site, is decreased while phosphorylation of Src at Tyr 527, the inhibition site, is increased. GAPDH equal loading control remains unchanged. (B) Phosphorylation of JNK at Thr183/Tyr185, p38MAPK at Thr180/Tyr182 and pERK1/2 at Thr202/Tyr204 is decreased in both cell lines with knockdown of Cav-1, consistent with global reduction in proliferative pathways. Totals remain unaffected. DUSP5 levels are increased in both cell lines concomitantly. GAPDH shows equal loading control. (C) Schematic depicting the pathways affected in signaling when Cav-1 is downregulated in pancreatic cancer cell lines.