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. Author manuscript; available in PMC: 2011 Jul 1.

Published in final edited form as: Int J Cancer. 2010 Jul 1;127(1):32–42. doi: 10.1002/ijc.25029

Sodium selenite activated JNK1 (increase of phosphorylated JNK1, p-JNK1) and inhibited β-catenin signaling in dose- and time-dependent manner in colon cancer cells HCT116 (A and B) and SW620 (C and D), respectively. “C” referred as “control”, and “T” referred as “sodium selenite treatment”. β-actin was used as loading control. The image signal of p-JNK1 and β-catenin was quantified and normalized to β-actin. The ratio was presented. These experiments were triplicated independently.

Sodium selenite activated JNK1 (increase of phosphorylated JNK1, p-JNK1) and inhibited β-catenin signaling in dose- and time-dependent manner in colon cancer cells HCT116 (A and B) and SW620 (C and D), respectively. “C” referred as “control”, and “T” referred as “sodium selenite treatment”. β-actin was used as loading control. The image signal of p-JNK1 and β-catenin was quantified and normalized to β-actin. The ratio was presented. These experiments were triplicated independently.