Table 1. Up-regulated PRA–target genes in the presence of P4.
Class | Gene | Name | FC | FI | Function |
---|---|---|---|---|---|
A+&AB+ | DUSP6 | Dual specificity phosphatase 6 | 2 | 1.5 | Transcriptional target of P53 Interaction with PRB: proliferative transcriptional programs |
A+&AB+ | BCL 2 -L 1 | Bcl-2-like protein 1 | 1.5 | 1.2 | Overexpression of Bcl-xL: loss of apoptosis |
A+&AB+ | TNFRSF11A | Receptor Activator of Nuclear Factor κ B (RANK) | 1.9 | 1.6 | Mammary cell proliferation, migration, cell invasion. |
A+&AB+ | WNT5A | Wingless-type MMTV integration site family, member 5A | 1.8 | 1.3 | Tumor suppressor gene Proliferation, differentiation, migration, adhesion, polarity |
A+&AB+ | LGR4 | Leucine-rich repeat-containing G-protein coupled receptor 4 (GPR48) | 1.8 | 1.6 | Promoting cancer cell proliferation (Wnt signaling), Invasiveness and metastasis |
A+&AB+ | FOSB | FBJ murine osteosarcoma viral oncogene homolog B | 1.8 | 1.5 | Reduced FosB expression: dedifferentiation (breast tumorigenesis) |
A+&AB+ | TFPI2 | Tissue factor pathway inhibitor 2 | 2.2 | 2.6 | Low expression: breast cancer progression and poor outcome |
A+&B+ & AB+ | DUSP1 | Dual specificity phosphatase 1 | 1.6 | 1.6 | Cell cycle, dephosphorylation of MAP kinase. Antiproliferative actions of PR |
MDA-iPRAB cells were cultured during 24 h in steroid-free medium containing RSL1 (0.5 μM) and/or Dox (2 μM) to induce expression of PRA and/or PRB. Cells were treated by vehicle or P4 (1 nM) for 6 hours and a genome wide transcriptomic studies was performed as described in [6]. A total of 999 genes were affected by PR expression. These genes were separated into three groups: A and B and AB (co-expressed at similar levels relative to physiological conditions) regrouping genes that are regulated by either by PRA, PRB or PRAB. Tables above represent class A+ genes regulated by PRA in the presence of the ligand; Class A+&AB+, genes responsive to liganded PRA and their expression may or may not be influenced by PRB co-expression; Class A±&AB± genes responsive to both liganded and unliganded PRA, and their expression may be influenced by PRB co-expression; Class A+&B+& AB+, genes that are commonly regulated by liganded PRA, PRB and PRAB. FC calculated either by microarray studies or by RT-qPCR analysis and their function in the cancer. FC: Transcriptional Fold Change calculated by microarray studies (FC*) and by RT-qPCR (FI, Fold Induction).