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Molecular mechanism through which PPARγ counteracts leptin expression and function in breast cancer. Leptin, through JAK/STAT/MAPK activation, increases GR phosphorylation (pGR) and its nuclear translocation. pGR transactivates leptin promoter by binding to GRE motif. In the presence of BRL, PPARγ binds to GRE and, through the formation of GR/PPARγ complex, allows the recruitment of NCoR and SMRT corepressors, thus inhibiting Ob transcription and reducing breast tumor growth.
