Associations between intratumoral CD68-positive and patients' clionicaopathologic characteristics.

<p>Associations between intratumoral CD68-positive and patients' clionicaopathologic characteristics.</p

Macrophage Infiltration Induces Gastric Cancer Invasiveness by Activating the β-Catenin Pathway - Fig 6

<p>(A) Effect of macrophage CM on mRNA and protein expression of β-catenin down-stream genes. N87 cells were cultured in the presence or absence of macrophage CM. For RNA and protein level, cells were collected after 6 hours and 24 hour treatment respectively. (B) N87 cells with or without knock-down of β-catenin utilizing shRNA-2 were co-treated in the presence or absence of macrophage CM. N87 cells were collected after 24 hours treatment and analyzed with western blot. (C) Effect of MMP7 neutralized antibody on GC cells invasion. N87 cells in the presence of macrophage CM for 24 hours were pre-treated with various doses MMP7 neutralized antibody (0, 0.625, 1.25 and 2.5μg/ml) for 1 hour Isotype IgG was used as a blocking control. (D) Effect of CD44 neutralized antibody on GC cell invasion. N87 cells in the presence of macrophage CM for 24 hours were pre-treated with various doses CD44 neutralized antibody (0, 1.25, 2.5, 5 and 10 μg/ml) for 1 hour. Isotype IgG was used as a blocking control. All data represent the arithmetic mean ± SEM. * <i>p</i> < 0.05.</p

Immunohistochemistry analysis.

<p>β-catenin was highly expressed in tumors. (A) In most cases, β-catenin expression was primarily located in the cytoplasm. However, (B) strong nuclear staining of β-catenin in GC cells was positively associated with CD68+ macrophages in the tumor lesions.</p

Macrophage Infiltration Induces Gastric Cancer Invasiveness by Activating the β-Catenin Pathway - Fig 4

<p>(A) Migration activity of THP-1 monocyte co-cultured with different gastric cancer cell lines (AGS, N87, MKN-45 and TSGH). THP-1 monocyte will be recruited by different gastric cancer cell lines and the recruiting ability is dependent on the degree of malignancy. (B) Invasion ability of GC cells treated by macrophage CM. Four different types of GC cells (AGS, MKN45, N87 and TSGH) were seeded in a Boyden chamber and co-cultured with or without macrophage cells or macrophage CM for 24 hours. Invasion abilities of each cell line were measured <i>in vitro</i> for 24 hours. All data represent the arithmetic mean ± SEM. * p < 0.05, ** p < 0.01. (C) Effect of macrophage CM co-cultured with cells. N87 and AGS cells were co-cultured with macrophage CM respectively for 24 hours and cell viability was determined by MTT assay.</p

Effect of macrophage CM on β-catenin pathway.

<p>(A) β-catenin accumulates in nucleus after treatment with macrophage CM for 30 minutes in N87 cells. (B) Immunofiuorescent images were observed with a confocal microscope. β-catenin positive cells were analyzed by using an anti-β-catenin antibody, which is recognized by secondary rabbit antibody conjugated with FITC, depicted by green fluorescence; Nuclear staining was detected by counterstaining cells with 4', 6-Diamidino-2-phenylindole (DAPI), represented as blue fluorescence. Co-culturing with macrophage CM, immunofiuorescence staining showed β-catenin-FITC complexes translocated into nucleus. (C) Invasion ability of GC cells treated by macrophage CM.</p

Kaplan-Meier overall survival curves for gastric cancer patients as TAM density (Low: TAM<671, blue line; High: TAM>671, brown line; <i>p</i> = 0.0073).

<p>Kaplan-Meier overall survival curves for gastric cancer patients as TAM density (Low: TAM<671, blue line; High: TAM>671, brown line; <i>p</i> = 0.0073).</p

Immunohistochemistry analysis.

<p>Immunostaining against CD68 was performed on tissue slides from gastric cancer patients. CD68+ macrophage staining was sparse in the normal gastric mucosa (A). CD68+ cells were detected in both the stroma and tumor nest (B & C). The density of CD68+ macrophages in pathological tumor staging (pT) 1 (D) and pT4 (E) tumor lesions.</p

Distribution frequency of vascular endothelial growth factor (VEGF)-C genotypes in 310 controls and 166 patients with urothelial cell carcinoma (UCC) without tobacco consumption.

<p>Odds ratios (ORs) and their 95% confidence intervals (CIs) were estimated by logistic regression models. Adjusted ORs (AORs) and their 95% CIs were estimated by multiple logistic regression models after controlling for age and gender.</p><p>*<i>p</i><0.05, statistically significant.</p

Additional file 1: of Targeting the SPOCK1-snail/slug axis-mediated epithelial-to-mesenchymal transition by apigenin contributes to repression of prostate cancer metastasis

Figure S1. Wound-healing assay of apigenin (API)-treated DU145 prostate cancer cells. Figure S2. Migration and Matrigel invasion assay of DU145 cells using a Transwell system. Figure S3. SPOCK1 is critical for apigenin (API)-modulated invasiveness of prostate cancer cells. Figure S4. Akt is a downstream regulator of SPOCK1 to regulate Snail family expression in apigenin (API)-treated prostate cancer cells. Table S1. Normalization of wound healing, cell invasion and migration to cell viability under API treatment. (DOCX 1043 kb

Distribution frequencies of vascular endothelial growth factor (VEGF)-C genotypes in 210 controls and 67 patients with urothelial cell carcinoma (UCC) who consumed tobacco.

<p>Odds ratios (ORs) and their 95% confidence intervals (CIs) were estimated by logistic regression models. Adjusted ORs (AORs) and their 95% CIs were estimated by multiple logistic regression models after controlling for age and gender.</p><p>*<i>p</i><0.05, statistically significant.</p