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Roles and mechanisms for PI-88 in esophageal tumor growth and angiogenesis: Evaluation in nude mouse model created by coinjection of tumor cells with matrigel
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Abstract:
Objective: To create a mouse xenograft model of esophageal squamous cancer by coinjection of tumor cells with matrigel and to determine the anti-tumor and anti-angiogenic effects of PI-88 using this model. Methods: Nude mice were co-injected with human esophageal cancer TE-13 cells and matrigel subcutaneously. They were then randomized to receive subcutaneously physical saline (n=4, 20 ml/\[kg?day\]) as controls and PI-88 (n=4, 20 mg/\[kg?day\]) as test treatment, respectively. At day 2, 6, 10, 14 d after the last dose, contrast enhanced CT scans were performed on the xenograft region and xenograft tumor specimens were collected for analyses of heparanase (HPSE) and vascular endothelial growth factor(VEGF), respectively, by S-P staining and histoimmunological staining. Results: Xenograft tumors were formed on the same day of tumor cell injection in 8 mice. On post-treatment d 14, the volume of xenograft tumors was significantly reduced in the PI-88 treatment group (70.25±6.85 mm3) than in the I-88 treatment group (143.13±1718) (P<0.05). On d 15, CT value was significantly lower in the PI-88 treatment group (15.18±0.91 mm2) than in the control group (19.23±2.03 mm2) (P<0.05), and staining signals for both HPSE (28.70±6.39 vs 87.55±22.03, P<0.01) and VEGF (47.10±8.18 vs 94.40±14.47, P<0.01) in the control group than in the treat group. Conclusions: Co-injection of xenograft tumor cells with matrigel may offer a reliable and more efficient approach of establishing animal models of esophageal cancer. PI-88 may inhibit esophageal tumor growth and angiogenesis, possibly, through VEGF- and HPSE-dependent mechanisms.
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Project Supported:
Project supported by the Science Research Foundation from the Bureau of Health of Hebei Province（No. 20120130）
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