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Aryl hydrocarbon-estrogen alpha receptor-dependent expression of miR-206, miR-27b, and miR-133a suppress cell proliferation and migration in MCF-7 cells.

Keivan MobiniGholamhossein TamaddonReza FardidMajid KeshavarziAfshin Mohammadi-Bardbori
Published in: Journal of biochemical and molecular toxicology (2019)
The underlying functions of miR-206, miR-133a, miR-27b, and miR-21, and their link to the estrogen receptor alpha (ERα) and aryl hydrocarbon receptor (AhR) signaling pathways remain largely unexplored. In this study, we detect the expression of miR-206, miR-133a, miR-27b, and miR-21 in MCF-7 through quantificational real-time polymerase chain reaction assay along with the activation/inhibition of ERα and AhR receptors. Aside from this, cell proliferation and migration as well as AhR-dependent CYP1A1 enzyme activity were measured. Here, we found that the forced increased expression of miR-206, miR-133a, and miR-27b were closely associated with the suppression of MCF-7 cell proliferation and migration. The anti-proliferative-metastatic effect of miR-206, miR-133a, and miR-27b was probably mediated by targeting the ERα and AhR signaling pathways. Considered together, our study indicated that the overexpression of miR-206, miR-133a, and miR-27b might be potential biomarkers for prognosis and therapeutic strategies in breast cancer.
Keyphrases
  • cell proliferation
  • long non coding rna
  • long noncoding rna
  • poor prognosis
  • estrogen receptor
  • squamous cell carcinoma
  • stem cells
  • cell death
  • transcription factor
  • young adults
  • cell therapy
  • bone marrow