title: MicroRNA-153 Regulates NRF2 Expression and is Associated with Breast Carcinogenesis.
abstract: BACKGROUND
  Abnormal expression of NRF2 levels in some tumor tissues may enhance drug resistance through various mechanisms. Recent studies have demonstrated a link between dysregulated expression of miRNAs and breast carcinogenesis.
  
  
  METHODS
  Quantitative RT-PCR analysis was used to examine the expression levels of miR-153 in breast cancer cell lines. The biological effects of miR-153 were assessed in CRC cell lines using clonogenic cell survival assay, mammosphere formation assay, cell migration assay, 8-OHdG estimation assay, and flow cytometry analysis. Quantitative RT-PCR and western blot analyses were employed to evaluate the expression of miR-153 targets. In this study, we investigated the role of vitamin C in the regulation of miR-153 (miR-153) and its target gene(s) in cell models of mammary carcinogenesis.
  
  
  RESULTS
  In human breast cell lines treated with E2, the level of miR-153 was found to be increased. In contrast, vitamin C treatment was able to decrease the expression of miR-153. Bioinformatic prediction indicates nuclear factor erythroid 2-related factor 2 (NRF2) may be a target for miR-153. In E2-treated breast cancer cell lines, NRF2 protein level was found to be decreased. Overexpression of miR-153 significantly reduced NRF2 and the downstream genes. Furthermore, miR-153 was found to decrease apoptosis and increase colony formation in breast epithelial cells.
  
  
  CONCLUSIONS
  These data indicate that miR-153 acts as an oncogene in breast carcinogenesis by targeting NRF2.
authors.forename: Bo
authors.initials: B
authors.lastname: Wang
authors.forename: Yang
authors.initials: Y
authors.lastname: Teng
authors.forename: Qilun
authors.initials: Q
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis; D001205:Ascorbic Acid / Q000494:pharmacology; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D019295:Computational Biology; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008321:Mammary Glands, Animal / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism*; D018384:Oxidative Stress; D034622:RNA Interference; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D014162:Transfection
chemical_list: C556500:MIRN153 microRNA, human; C000606654:MIRN153 microRNA, rat; D035683:MicroRNAs; D051267:NF-E2-Related Factor 2; C495635:NFE2L2 protein, human; C495637:Nfe2l2 protein, rat; D004958:Estradiol; D001205:Ascorbic Acid