In the article by Zhang and colleagues on the role of COX-2 in TPA-induced cell transformation in the January 2008 issue of Molecular Cancer Research, Chuanshu Huang's affiliation was incorrect. It is Nelson Institute of Environmental Medicine, New York University School of Medicine, New York, NY.

Errors were also found in the β-actin bands of Figures 4E and 6F and the cropped bands of COX-2 and β-actin in Figure 2D. The corrected figures appear here:

FIGURE 2D.
FIGURE 2D. C141 cells were transfected with human COX-2 expression vector or exposed to TPA (20 ng/ml) for 12 hrs as indicated. COX-2 protein expression was evaluated by Western blotting using specific antibodies against COX-2. β-Actin was used as protein loading control.
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C141 cells were transfected with human COX-2 expression vector or exposed to TPA (20 ng/ml) for 12 hrs as indicated. COX-2 protein expression was evaluated by Western blotting using specific antibodies against COX-2. β-Actin was used as protein loading control.

FIGURE 2D.
FIGURE 2D. C141 cells were transfected with human COX-2 expression vector or exposed to TPA (20 ng/ml) for 12 hrs as indicated. COX-2 protein expression was evaluated by Western blotting using specific antibodies against COX-2. β-Actin was used as protein loading control.
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C141 cells were transfected with human COX-2 expression vector or exposed to TPA (20 ng/ml) for 12 hrs as indicated. COX-2 protein expression was evaluated by Western blotting using specific antibodies against COX-2. β-Actin was used as protein loading control.

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FIGURE 4E.
FIGURE 4E. WT, JNK1-/- and JNK1-/-(HA-JNK1) MEFs were treated with TPA for 6 hrs, and the cell extracts were subjected to Western blotting using specific antibody against COX-2. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.
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WT, JNK1-/- and JNK1-/-(HA-JNK1) MEFs were treated with TPA for 6 hrs, and the cell extracts were subjected to Western blotting using specific antibody against COX-2. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.

FIGURE 4E.
FIGURE 4E. WT, JNK1-/- and JNK1-/-(HA-JNK1) MEFs were treated with TPA for 6 hrs, and the cell extracts were subjected to Western blotting using specific antibody against COX-2. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.
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WT, JNK1-/- and JNK1-/-(HA-JNK1) MEFs were treated with TPA for 6 hrs, and the cell extracts were subjected to Western blotting using specific antibody against COX-2. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.

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FIGURE 6F.
FIGURE 6F. WT and DN-MKK4+7 cells were treated with TPA for 60 min. The extracts were subjected to Western blotting with specific antibodies as indicated. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.
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WT and DN-MKK4+7 cells were treated with TPA for 60 min. The extracts were subjected to Western blotting with specific antibodies as indicated. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.

FIGURE 6F.
FIGURE 6F. WT and DN-MKK4+7 cells were treated with TPA for 60 min. The extracts were subjected to Western blotting with specific antibodies as indicated. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.
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WT and DN-MKK4+7 cells were treated with TPA for 60 min. The extracts were subjected to Western blotting with specific antibodies as indicated. β-Actin was used as protein loading control. Lanes irrelevant to the figure have been cropped as indicated.

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Zhang D, Li J, Song L, Ouyang W, Gao J, Huang C. A JNK1/AP-1-dependent, COX-2 induction is implicated in 12-O-tetradecanoylphorbol-13-acetate-induced cell transformation through regulating cell cycle progression. Mol Cancer Res 2008;6:165–74.

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© 2009 American Association for Cancer Research.
2009