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Figure 8 | Molecular Cancer

Figure 8

From: Stimulation of neoplastic mouse lung cell proliferation by alveolar macrophage-derived, insulin-like growth factor-1 can be blocked by inhibiting MEK and PI3K activation

Figure 8

MØCM IGF-1 content regulates the proliferation of treated neoplastic cells. A-B: Macrophage-conditioned media (MØCM) was concentrated and immunoprecipitated against isotype control (Con IgG) or α-mIGF-1 IgG antibodies (α-IGF IgG). (A) Media IGF-1 content was analyzed by ELISA, and (B) LM2 or JF32 cells were cultured in serum-free media with 0.5% BSA, with or without the MØCM generated in (A). Relative growth was determined by MTS, and mean + SD plotted as fold-change from control, which was normalized to 1.0. Data was pooled from at least 3 independent experiments. * P < 0.01 vs. Con IgG; ** P < 0.001 versus untreated cells, and ## P < 0.001 versus the Con IgG group by 1-way ANOVA. C-D: (C) IGF-1 concentration in media conditioned by macrophages pre-treated with scrambled control siRNA (scr siRNA) or α-IGF-1 siRNA construct, vs. naïve MØCM, was determined by ELISA; (D) LM2 or JF32 cells were cultured and relative cell number determined as in (C). (C) ** P < 0.001 vs. naïve MØCM and ## P < 0.001 versus the scr-siRNA by 1-way ANOVA; (D) ** P < 0.001 vs. untreated cells; # P < 0.05 and ## P < 0.001 vs. the scr siRNA group; and &P < 0.001 vs. the MØCM group by 1-way ANOVA. E-F: Pearson correlation and linear regression of MØCM IGF-1 levels from (C) vs. the fold-change in LM2 or JF32 cell number from (D) after MØCM addition; (E) LM2 P < 0.001 and (F) JF32 P < 0.0001.

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