TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000350375
  • Gene Name:PIT1
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:Northern blot
  • mRNA Pathway:VDR signaling pathway
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB00136 (NUTR00003, APRD00246, DB05314)
  • Drug Name:Calcitriol (1-alpha-25-Dihydroxyvitamin D3)
  • Drug Method:down-regulated the gene expression the gene expression

Disease basic infommation

  • Disease:breast cancer
  • Tissue:cell line (MCF-7)

Other information

  • Title:The vitamin D receptor represses transcription of the pituitary transcription factor Pit-1 gene without involvement of the retinoid X receptor
  • Journal:Mol Endocrinol
  • Published:2006
  • PubMed ID:16322098
  • Abstract:Pituitary transcription factor-1 (Pit-1) plays a key role in cell differentiation during organogenesis of the anterior pituitary, and as a transcriptional activator for the pituitary GH and prolactin genes. However, Pit-1 is also expressed in nonpituitary cell types and tissues. In breast tumors, Pit-1 mRNA and protein levels are increased with respect to normal breast, and in MCF-7 human breast adenocarcinoma cells, Pit-1 increases GH secretion and cell proliferation. We report here that 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] administration to MCF-7 cells induces a significant decrease in Pit-1 mRNA and protein levels. By deletion analyses, we mapped a region (located between -147 and -171 bp from the transcription start site of the Pit-1 gene) that is sufficient for the repressive response to 1,25-(OH)2D3. Gel mobility shift and chromatin immunoprecipitation assays confirmed the direct interaction between the vitamin D receptor (VDR) as homodimer (without the retinoid X receptor), and the Pit-1 promoter, supporting the view that Pit-1 is a direct transcriptional target of VDR. Our data also indicate that recruitment of histone deacetylase 1 is involved in this repressive effect. This ligand-dependent Pit-1 gene inhibition by VDR in the absence of the retinoid X receptor seems to indicate a new mechanism of transcriptional repression by 1,25-(OH)2D3.
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