MCT-1 gene and protein expressions are decreased by p53. The pGL3-MCT-1 promoter construct was transiently transfected into H1299 (p53 null) cells. (A) Reduced luciferase activity of the pGL3-MCT-1 reporter was identified when H1299 cells (control) expressed the wild-type p53 but not the mutant p53. Similar effects were recognized in context of MCT-1 overexpression (MCT-1) (B) The half-life (t1/2) of MCT-1 mRNA was analyzed by qRT-PCR after actinomycin D (5 μg/ml) treatment for the indicated time. Quantitative data was acquired as normalized with 18S rRNA levels. Cellular MCT-1 mRNA turnover was greater induced by p53 expression (control + p53) than p53 null condition (control). The exogenic MCT-1 mRNA decayed quickly in p53 renovation (MCT-1 + p53) versus (vs.) without p53 expression (MCT-1). (C) As determined with qRT-PCR analysis, the p53 knock-in H1299 moderately depressed intrinsic MCT-1 mRNA levels (control vs. control + p53). As well, the exogenic MCT-1 mRNA levels were significantly depressed by p53 (MCT-1 vs. MCT-1 + p53). (D) MCF-10A cells were under ETO genotoxic stress for 4 h. The ectopic (V5-tag) and intrinsic MCT-1 protein in MCF-10A (p53-proficient) cells were reversely elevated because p53 gene silence (p53 shRNA) relative to MOCK experiment. (E) Ectopic expression of MCT-1 reduced pGL3-MCT-1 promoter activity together with decrease in intrinsic MCT-1 protein. The overall cellular MCT-1 protein amounts (intrinsic plus ectopic) were more than a 2.2-fold elevation after MCT-1 induction. Statistics were analyzed with Student's t test. ***p < 0.0001.