Protein Kinase Cα Modulates Estrogen-Receptor-Dependent Transcription and Proliferation in Endometrial Cancer Cells
Figure 5
PKCα effects on ER-dependent transcription are mediated by the PI3-kinase/Akt pathway. (a) Ishikawa cells were transiently transfected with 0.5 μg pEREluc and 0.3 μg pCMVβ, in the presence or absence of 0.5 μg pmyrPKCα. (b) HEC-50 cells were transiently transfected with ERα (0.5 μg pHEGO), 0.5 μg pEREluc, and 0.3 μg pCMVβ ± 0.5 μg pmyrPKCα or pCDNA3. Cells were treated with ±100 nM estradiol (E2) in the presence or absence of the Akt and PI3K inhibitors, Akt-I-1/2 (1 μM) and LY29004 (10 μM), respectively. Promoter activity was determined as in Figure 2 and expressed as fold increase over the appropriate inhibitor or diluent control. Results are mean ± s.d. . *.
