Fig. 5.
Fig. 5. The GR antagonist RU486 fully reversed the LCL growth-promoting effects and RA antagonism mediated by glucocorticoids. / (A) DAA-3 cells were incubated in SFM (CTR, control) for the indicated times with or without RU486 (from 10−5 to 10−7 mol/L) in the presence or absence of 10−6 mol/L Dex (left panel) or 10−7mol/L HC (right panel). (B) The panel depicts the effects of different concentrations of RU486 (from 10−5 to 10−7 mol/L) on the antagonistic activity exerted by 10−6 mol/L Dex (left panels) or 10−7 mol/L HC (right panels) against DAA-3 and HDE-14 cell growth inhibition induced by 10−5 mol/L 13-cis-RA. Proliferation was evaluated at different time-points by 3H-thymidine uptake. The results of 1 representative experiment out of 3 are shown. Each point represents the mean plus or minus SD of values obtained from triplicate wells.

The GR antagonist RU486 fully reversed the LCL growth-promoting effects and RA antagonism mediated by glucocorticoids.

(A) DAA-3 cells were incubated in SFM (CTR, control) for the indicated times with or without RU486 (from 10−5 to 10−7 mol/L) in the presence or absence of 10−6 mol/L Dex (left panel) or 10−7mol/L HC (right panel). (B) The panel depicts the effects of different concentrations of RU486 (from 10−5 to 10−7 mol/L) on the antagonistic activity exerted by 10−6 mol/L Dex (left panels) or 10−7 mol/L HC (right panels) against DAA-3 and HDE-14 cell growth inhibition induced by 10−5 mol/L 13-cis-RA. Proliferation was evaluated at different time-points by 3H-thymidine uptake. The results of 1 representative experiment out of 3 are shown. Each point represents the mean plus or minus SD of values obtained from triplicate wells.

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