Fig. 2
From: NNAT is a novel mediator of oxidative stress that suppresses ER + breast cancer
NNAT mRNA expression is regulated by oxidative stress and activation of PPAR signaling cascade. A Luminescence activity of NNAT promoter activity co-transfected with E2F1, E2F4, NRF1, PPARα + RXR, PPARγ + RXR, or pLX304 control plasmid in ER + breast cancer cell lines. Data presented as mean percentage of GLuc/SEAP ratio normalized to pLX304 ± SEM (n = 9 per group; paired t-test, ***p < 0.001 vs. pLX304 control). B Evaluation of mRNA expression of NNAT, tumor suppressors genes CDKN1A and CDKN2B, and the transcription factor NRF1 responsible for cellular growth, during the exposure to H2O2. MCF10A, MDA-MB-231, T47D, and ZR75 cell lines untreated or treated with H2O2 (n = 3 per group; paired t-test, *p < 0.05, **p < 0.01, ***p < 0.001 vs. control). C NNAT mRNA expression of MCF10A, MDA-MB-231, T47D, and ZR75 cells treated with or without PPAR agonist, Clofibrate (n = 3 per group; paired t-test, *p < 0.05, **p < 0.01 vs. untreated control)