Fig. 5

CLPTM1L activates the promoter of ERβ-induced genes by stimulating ERβ in NSCLC cells. a–i Cells were transfected with relative plasmids and siRNAs, exposed to 4 Gy IR, followed by luciferase reporter gene assays. a ERE-LUC activity was examined using luciferase reporter gene assays in A549 and H460 cells transfected with pcDNA-CLPTM1L plasmids (E2, also called 17β-estradiol, was used as the positive control). b ERE-LUC activity was examined using luciferase reporter gene assays in A549 cells transfected with pcDNA-CLPTM1L plasmids or CLPTM1L siRNA. c ERE-LUC activity was determined using luciferase reporter gene assays in H460 cells treated with various doses of pcDNA-CLPTM1L plasmids. d The mutation of the ERE is shown in the ERE-LUC construct. e Luciferase reporter gene assays in A549 and H460 cells transfected with ERE-LUC constructs with wild-type or mutant ERβ-binding sites (E2 was used as the positive control). f ERE-LUC activity was detected by luciferase reporter gene assays in A549 and H460 cells transfected with pcDNA-CLPTM1L and ERβ siRNAs. g The effect of CLPTM1L on ERE-LUC activity was tested by luciferase reporter gene assays in ER-negative cells (MDA-MB-231) transfected with or without pcDNA-ERβ/pcDNA-ERα. NS, not significant. h ERE-LUC activity was detected by luciferase reporter gene assays in A549 and H460 cells transfected with pcDNA-ERβ and CLPTM1L siRNAs. i ERE-LUC activity was examined by luciferase reporter gene assays in A549 and H460 cells transfected with pcDNA-CLPTM1L and/or pcDNA-ERβ plasmids. All experiments were repeated at least three times. Student’s t test; * P < 0.05; ** P < 0.01; *** P < 0.001