Research Paper Volume 12, Issue 1 pp 611—627

Aspirin enhances the sensitivity of colon cancer cells to cisplatin by abrogating the binding of NF-κB to the COX-2 promoter

Figure 6. Aspirin synergizes the inhibiting effect of Cisplatin on tumor growth in a xenograft mouse model of human colon cancer cells. Human colon cancer LoVo cells (5×106, 5×105 in 100 ul PBS) were injected subcutaneously into the left and right flank of each athymic nude mice respectively. The four randomly assigned groups (n=6 for each group) were used: (1) non-drug therapy as negative control; (2) the treatment with Cisplatin (3 mg/kg) through intraperitoneal injection every three days; (3) a daily treatment of Aspirin(100 mg/kg) through intragastric administration; (4) the combination therapy of Cisplatin and Aspirin. (A) The representative images of the measurement of tumor diameters. (B) Dynamic development of tumor volume during the therapy. (C) Tumor weight of nude mice from each group at the moment when mice were sacrificed. (D) Images of xenograft tumor harvested after therapy. (E) The expression levels of β-catenin, N-Cadherin, Bcl-2, p-Akt(S473), p-p65, p-Erk1/2, COX-2, p65 and p50 in tumor tissue lysates were detected by western blot assay (n=6). (F) HE staining and immunohistochemical staining assay to show tissue morphological variations and the expressions of N-Cadherin, p-Akt(S473), p-p65, p-Erk1/2, COX-2, p65 and p50 in tissue sections. The representative images were taken by upright microscope. Scale bars, 100 μm (n=6). (G) Serum creatinine (Cr) and Blood Urea Nitrogen (BUN) levels of mice in each group were measured by the detection kit (n=6). Data were presented as means ± SD, *P<0.05, **P<0.01, ***P<0.001.