Figure 1From: CCR9-CCL25 interactions promote cisplatin resistance in breast cancer cell through Akt activation in a PI3K-dependent and FAK-independent fashionCCL25 inhibits cisplatin-induced reductions in cell growth. MDA-MB-231 cells were cultured with 0 or 100 ng/ml of CCL25 plus isotype control or anti-CCR9 Ab (1 μg/mL) for 24 hours, along with increasing concentrations of cisplatin (0-50 μg/mL). Cell proliferation was determined by BrdU incorporation in triplicate and was repeated 3 times. Asterisks (*) indicate significant differences (p < 0.01) between CCL25-treated and untreated BrCa cells.Back to article page