Fig. 4.

HI-B1 inhibits β-catenin-driven tumorigenesis in vivo.

(a) β-Catenin expression levels in colon cancer PDX samples were examined by immunohistochemistry (IHC) and its integrated optical density (IOD) was quantified using Image-Pro Plus software (v.6.1) program (Media Cybernetics, Bethesda, MD). Scale bar: 50 μm.

(b and c) HI-B1 was administered per os (p.o) (orally) three times a week at a dose of 50 mg/kg (n = 8/group) to JG5 (b) and JG14 (c) tumors. Tumor size was measured three times a week and the weight was measured at the end of experiments. (One-way ANOVA and Dunnett's test; *P < 0.05, significant difference compared to the vehicle group.)

(d) In the JG5 PDX tumor, c-Myc Expression level change by HI-B1 treatment was measured by IHC (same as Fig. 4A). Scale bar: 50 μm.

(e) HI-B1 reduced polyp formation driven by aberrant activation of β-catenin in APC^min mouse model. The indicated doses of HI-B1 were administered p.o. for 10 weeks, and mice were sacrificed for analysis of intestinal carcinogenesis (n = 6/group).

(f and g) Small intestine tissue was prepared from the same position of ileum from mice, and then mRNA expression levels of c-myc (f) and cyclin D1 (g) were quantified by qRT-PCR. (One-way ANOVA; *P < 0.05, **P < 0.01, significant difference compared to the vehicle group.)