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Breast cancer is a leading cause of cancer‐related death in women. Prolonged exposure to the ovarian hormones estrogen and progesterone increases the risk of breast cancer. Although estrogen is known as a primary factor in mammary carcinogenesis, very few studies have investigated the role of progesterone. Receptor activator for nuclear factor‐κB ( NF ‐κB) ligand ( RANKL ) plays an important role in progesterone‐induced mammary carcinogenesis. However, the molecular mechanism underlying  RANKL ‐induced mammary carcinogenesis remains unknown. In our current study, we show that  RANKL  induces glioma‐associated oncogene homolog 1 ( GLI ‐1) in estrogen‐induced progesterone‐mediated mammary carcinogenesis.  In vivo  experiments were carried out using  ACI  rats and  in vitro  experiments were carried out in  MCF ‐7 cells. In  ACI  rats, mifepristone significantly reduced the incidence of mammary tumors. Likewise, mifepristone also inhibited the proliferation of  MCF ‐7 cells. Hormone treatments induced  RANKL , receptor activator of  NF ‐κB (RANK), and  NF ‐κB in a protein kinase B‐dependent manner and inhibited apoptosis by activation of anti‐apoptotic protein Bcl2 in mammary tumors and  MCF ‐7 cells. Mechanistic studies in  MCF ‐7 cells reveal that  RANKL  induced upstream stimulatory factor‐1 and  NF ‐κB, resulting in subsequent activation of their downstream target  GLI ‐1. We have identified that progesterone mediates estrogen‐induced mammary carcinogenesis through activation of  GLI ‐1 in a  RANKL ‐dependent manner.

Receptor activator for nuclear factor‐κB ligand signaling promotes progesterone‐mediated estrogen‐induced mammary carcinogenesis