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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Mol Cancer Ther. 2015 Apr 8;14(6):1476–1487. doi: 10.1158/1535-7163.MCT-15-0030

Figure 2. CRY2 regulates colon cancer chemoresistance.

Figure 2

(A) Knockdown of CRY2 accelerates apoptosis induced by oxaliplatin. DLD-1 and SW480 cells were treated with increasing concentrations of oxaliplatin from 0.25 to 80μM after transfected with siCRY2 or control. The proportion of viable cells upon transduction with siCRY2 dropped more rapidly than in the control cells.

(B) Down-regulation of CRY2 expression enhances the pro-apoptotic effects of oxaliplatin on DLD-1 and SW480 cell line. Binding of Annexin V and uptake of propidium iodide were analyzed by flow cytometry. The mean of three data sets was taken and calculated from the corresponding quadrants (bar graphs, right panel). Error bars represent 95% confidence intervals. Treatment of 4μM oxaliplatin dramatically increased the portion of Annexin V+PI+/Annexin V+PI− in DLD-1 cells and SW480 transduced with siCRY2.

(C) CRY2 knockdown leads to increased poly-(ADP-ribose)polymerase (PARP) cleavage. DLD-1 cells transfected with siCRY2 or control siRNA were treated with or without 4μM oxaliplatin for 48 hours. Cell lysates were immunoblotted with indicated antibodies. CRY2 overexpression reduced cleavage of PRAP. DLD-1 cells transfected with myc-CRY2 or control vector were treated with or without 4μM oxaliplatin for 48 hours. Cell lysates were immunoblotted with indicated antibodies.

(D). TUNEL assay of DLD-1 and SW480 cell line. Cells transfected with control, or SiCRY2 were assayed for TUNEL signals. TUNEL positive cells were measured and presented as bar graphs. (**, P<0.01, n=3 experiments)