Fig. 5: Overexpression of a dominant negative form of STAT3 attenuates TLR4 signaling-mediated melanoma progression in mice.
From: Activation of STAT3 is a key event in TLR4 signaling-mediated melanoma progression
a Representative images (left panel) and weights (right panel) of B16NC and B16STAT3β tumors (n = 7, two independent experiments). b Immunoblot analyses of phosphorylated STAT3 (p-STAT3) in B16NC and B16STAT3β tumors. Representative immunoblotting results are shown in the left panel. Relative protein levels of p-STAT3 in tumors are shown in the right panel. The protein level of p-STAT3 in B16NC tumors without LPS stimulation was regarded as 1. c Representative IHC staining results of Ki-67, CD31, E-cadherin, N-cadherin and vimentin in B16NC and B16STAT3β tumors. Scale bar: 200 μm. d Flow cytometric analyses of splenic immune cells and tumor-infiltrating immune cells in the melanoma-bearing mice. Representative flow cytometry plots are shown in the left panels. Percentages of splenic MDSCs and CD8 T cells, and tumor-infiltrating CD8 T and NK cells are shown in the right panels. Data are shown as the mean ± SD. *P < 0.05 vs. the B16NC tumor group without LPS stimulation. #P < 0.05, ##P < 0.01 vs. the LPS-stimulated B16NC tumor group.
