Fig 1: Effect of FGF18 on the expression levels of ERK, p-ERK and c-Myc in MDA-MB-231 cells. (A and B) FGF18 induced the activation of the ERK pathways in MDA-MB-231 cells. The expression of ERK and p-ERK was evaluated by western blotting. The relative protein expression level of p-ERK was quantified in MDA-MB-231 cells. Each assay was performed in triplicate. (C and D) c-Myc protein levels were determined using western blotting and quantification is illustrated by a bar chart. (E) The CCK-8 assay revealed that 10 µmol/l ERK inhibitor (FR180204) inhibited the proliferation of MDA-MB-231 cells treated with 50 ng/ml FGF18. (F and G) The effect of FGF18 and FGF18+FR180204 on the expression levels of c-Myc in MDA-MB-231 cells. Data are presented as the mean ± standard deviation; *P<0.05 vs. the control. FGF18, fibroblast growth factor 18.
Fig 2: Effect of FGF18 on the regulation of the proliferation and cell cycle of MDA-MB-231 cells. (A) The CCK-8 assay revealed that FGF18 promoted MDA-MB-231 cell proliferation. (B and C) The colony-forming ability of cells treated with FGF18 compared with NC. The colony number was normalized to cells without any other treatment, which was set to 100%. (D and E) FGF18 increased the percent of G0/G1 phase and decreased the percent of S phase of MDA-MB-231 cells. The cell cycle of MDA-MB-231 cells was detected using flow cytometry. Data are presented as the mean ± standard deviation from three independent experiments. *P<0.05. FGF18, fibroblast growth factor 18.
Fig 3: Effect of siFGF18 on the regulation of proliferation of MDA-MB-231 cells. (A) The CCK-8 assay revealed that siFGF18 inhibited MDA-MB-231 cell proliferation. (B and C) The colony-forming ability of siFGF18-transfected MDA-MB-231 cells compared with FGF18-NC. The colony number was normalized to cells without any other treatment, which was set to 100%. (D and E) The cell cycle of MDA-MB-231 cells was detected using flow cytometry. (F and G) ERK, p-ERK and c-Myc protein levels were determined using western blotting and quantification is illustrated by a bar chart. Data are presented as the mean ± standard deviation from three independent experiments; *P<0.05. FGF18, fibroblast growth factor 18; siFGF18, short interfering RNA against fibroblast growth factor 18.
Fig 4: FGF18 siRNA inhibits the expression of FGF18. MDA-MB-231 cells were cultured in 6-well plates and were transfected with FGF18 siRNA. (A) Reverse transcription-quantitative polymerase chain reaction analysis of the expression of FGF18 mRNA. (B and C) Western blot analysis of the FGF18 protein expression was performed 48 h following transfection. *P<0.05 vs. FGF18-NC. siRNA, short interfering RNA; FGF18, fibroblast growth factor 18.
Fig 5: Wnt/ß-catenin signaling in the uterus at the pre-implantation period. The mRNA expression of Wnt4, Wnt5a, Wnt6, Wnt7A, Wnt7B, ß-catenin, and FGF18 in the uterus at E 3.5 was examined by quantitative-PCR in the control and M2(-) mice (A). Data were normalized to GAPDH mRNA levels to determine the relative abundance. The expression of ß-catenin and FGF18 protein in the uterus at the pre-implantation period in control and M2(-) mice at E3.5 was examined by immunohistochemistry. Rabbit IgG was used for negative control (B,C). Data are shown as the mean ± SEM. *p < 0.05.
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