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. Author manuscript; available in PMC: 2020 Mar 15.
Published in final edited form as: Mol Cell Endocrinol. 2018 Dec 20;484:78–92. doi: 10.1016/j.mce.2018.12.011

Fig-3: Effects of ERK1/2 and AKT pathways on proliferation of human endometriotic cells.

Fig-3:

Panel-1: The human endometriotic epithelial cells 12Z (Panel-1A) and stromal cells 22B (Panel-1B) were treated with MEK1/2 inhibitor (U0126, 0, 1, 10, 20, 50, 75, and 100 μM) to suppress ERK1/2 pathway and/or PI3K inhibitor (LY294002, 0, 1, 10, 20, 50, 75, and 100 μM) to suppress AKT pathway in vehicle (1% DMSO) in plain media for 24h. *- control vs. treatment, p<0.05, n=3. Panel-2A: The optimal concentration for was selected based on its effects on proliferation of 12Z and 22B cells. The 12Z cells and stromal cells 22B were treated with MEK1/2 inhibitor (U0126, 20μm) and/or PI3K inhibitor (LY294002, 50μm) for 24h. Panel-2B: ERK1 and AKT genes were silenced using siRNA approach. The number of live cells were counted at 48h post-transfection. In all experiments, the number of cells were counted using a Coulter counter and considered as 100% present in control. Data were expressed as mean ± SEM of three independent experiments conducted in duplicate. a- control vs inhibition of ERK1/2 pathway, b- control vs inhibition of AKT pathway, c- control vs. combined inhibition of ERK1/2 and AKT pathways, p<0.05, n=3. See Materials and Method section for additional experimental details.