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. 2013 Jan 24;104(3):337–344. doi: 10.1111/cas.12080

Figure 3.

Figure 3

Regulation of cyclin D1 by KRAS and c‐Jun N‐terminal kinase (JNK). (A) KP‐4 cells were transfected with control siRNA and cyclin D1 siRNA. Cell numbers were measured as in Fig. 2(A). Data are plotted as means ± SD of triplicate samples (*P < 0.05 vs. control siRNA‐transfected cells). (B) KP‐4 cells were transfected with the pcDNA3.1 or RasG12V vector together with pD1luc (left) or AP‐1luc (right) for 24 h. SP600125 (SP) or control vehicle (dimethylsulfoxide [DMSO]) was added to the supernatant immediately after the transfection. The ratio of reporter luciferase activity to the Renilla luciferase control is indicated. Results represent the means ± SD of triplicate samples (*P < 0.05). (C) KP‐4 cells were treated with control vehicle or SP600125 (SP) (left), or transfected with control, JNK1, JNK2, or both JNK1 and 2 siRNAs (right). After 48 h, relative mRNA levels of cyclin D1 were measured by real‐time reverse transcription‐polymerase chain reaction (RT‐PCR). Data are plotted as means ± SD of triplicate samples (*P < 0.05 vs. control siRNA‐transfected cells). Experiments were performed three times, and representative results are shown. (D) Human normal pancreas (n = 4, left) and pancreatic cancer sections (n = 20, right) were stained for cyclin D1 and representative images are shown (original magnification ×200, bar 100 μm). Insets show detailed areas containing pancreatic duct (original magnification ×400, bar 25 μm). Results are means ± SD of six random views (*P < 0.05).