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. 2008 Dec;19(12):2437–2446. doi: 10.1681/ASN.2008040394

Figure 5.

Figure 5.

CNI-mediated downregulation of CXCR3-B is associated with increased proliferation and migration of human renal cancer cells. (A and B) REC and 786-0 cells were treated with either different concentrations (0.01 to 1.00 μg/ml) of CsA or vehicle alone for 72 h. Some cells from both CsA-treated and the vehicle-treated group were incubated with CXCL4 (1.0 μg/ml) in the last 24 h. All of the cells in A and B were subjected to cell proliferation assay by measuring [3H]thymidine incorporation within the cells as described in the Concise Methods section. Data reflect three independent experiments. Columns are average of triplicate readings (cpm) of the samples; bars are ±SD. (C) The effects of CsA and CXCL4 on renal cancer cell migration were tested by in vitro wound-healing assay, as described in the Concise Methods section. Confluent monolayers of 786-0 cells were scarred, and repair was monitored microscopically after 36 h of treatment with CsA (0.1 and 1.0 μg/ml), or CXCL4 (1.0 μg/ml), CsA (1.0 μg/ml) + CXCL4 (1.0 μg/ml), or vehicle alone. The right panel represents the quantification of distance migrated by the cells in 36 h relative to vehicle-treated control cells in 0 h. Representative and average readings of three independent experiments; bars are ±SD. In *P < 0.05 versus vehicle-treated cells.