Fig. 5.

FGF9 stimulated tumor growth, angiogenesis, EMT, M2 macrophage infiltration and tumor metastasis of lung carcinoma in vivo. LLC cells subcutaneously injected C57BL/6 mice were treated with 25 ng/ml FGF9 or 0.00125% BSA (vehicle control) once daily for 16 days. Mice in Control (Con) group were subcutaneously inoculated with LLC cells and received no treatment. (A) Tumor growth curves were plotted against time. (B) Photograph and (C) weights of excised subcutaneous LLC tumors from the Control, BSA and FGF9 group mice at the time mice were sacrificed. (D) Immunohistochemical assays of Ki-67 and cleaved Caspase-3 (c-Casp3) expressions in the LLC subcutaneous injected tumors from various groups (original magnification, Ki67: × 200; c-Casp3: x100). (E) Photograph and (F) weight of excised liver and lung tissues of the FGF9, BSA or Control (Con) mice. (G) Immunohistochemical assays of CD31, E-cadherin, and N-cadherin, and M1 (iNOS) and M2 (Arg1) expressions in the LLC subcutaneous tumors from FGF9, BSA or Control mice (original magnification, CD31: x100, E-Cadherin, N-Cadherin, M1 and M2: x200). Values are represented as the mean ± SEM; n=6. The data were analyzed by two-way ANOVA with Sidak's multiple comparisons post-tests in (A) or one-way ANOVA with Tukey's multiple comparisons post-tests in (C), (D), (F) and (G); ^♯p<0.05, ^♯♯p<0.01 and ^♯♯♯p<0.001 vs. the Control group; *p<0.05, **p<0.01 and ***p<0.001 vs. the BSA group.