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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2013 Oct 3;273(2):10.1016/j.taap.2013.09.021. doi: 10.1016/j.taap.2013.09.021

Figure 3.

Figure 3

Treatment of human skin cancer cells with PGE2 stimulates β-catenin signaling and induces cell viability. (A) Cells were treated with PGE2 for 24 h and thereafter cells were harvested and nuclear lysates were prepared to detect the levels of nuclear β-catenin. Total cell lysates were used for the analysis of cell cycle regulatory proteins using western blot analyses. β-actin served as the loading control. (B) Effect of PGE2 on cell proliferation of skin cancer cells. Briefly, 5×104 cells were plated in six-well culture dishes and treated with PGE2 (10 μM) for 24 h. After 24 h, cells were harvested and counted using a microscope. The numbers of cells were compared between PGE2-treated and non-PGE2-treated groups. Significant increases vs non-PGE2-treated cells, *P<0.01. (C) Treatment of cells with an EP2 antagonist (AH6809) for 24 h inhibits nuclear accumulation of β-catenin in a concentration-dependent manner. (D) Treatment of A431 or SCC13 cells with EP2 antagonist inhibits the viability or proliferation of skin cancer cells. Significant inhibition of cell viability vs control cells, *P<0.01.