pRb controls Estrogen Receptor alpha protein stability and activity
Copyright policy )pRb controls Estrogen Receptor alpha protein stability and activity
A cross talk between the Estrogen Receptor (ESR1) and the Retinoblastoma (pRb) pathway has been demonstrated to influence the therapeutic response of breast cancer patients but the full mechanism remains poorly understood. Here we show that the N-terminal domain of pRb interacts with the CD domain of ESR1 to allow for the assembly of intermediate complex chaperone proteins HSP90 and p23. We demonstrated that a loss of pRb in human/mouse breast cells decreases the expression of the ESR1 protein through the proteasome pathway. Our work reveals a novel regulatory mechanism of ESR1 basal turnover and activity and an unanticipated relationship with the pRb tumor suppressor.
- Temple University United States
- Ca Foscari University of Venice Italy
- University of Siena Italy
- Department of Medicine Italy
Mice, Knockout, Proteasome, Breast cancer; Chaperone proteins; Estrogen receptor alpha; Prb; Proteasome, Protein Stability, Animals; Breast Neoplasms; Cell Line, Tumor; Estrogen Receptor alpha; Female; Humans; MCF-7 Cells; Mice; Mice, Knockout; Protein Stability; Receptor Cross-Talk; Retinoblastoma Protein; Tumor Cells, Cultured, Estrogen Receptor alpha, Breast Neoplasms, Receptor Cross-Talk, Retinoblastoma Protein, Chaperone protein, Mice, Breast cancer, Prb, Cell Line, Tumor, MCF-7 Cells, Tumor Cells, Cultured, Estrogen receptor alpha, Animals, Humans, Female
Mice, Knockout, Proteasome, Breast cancer; Chaperone proteins; Estrogen receptor alpha; Prb; Proteasome, Protein Stability, Animals; Breast Neoplasms; Cell Line, Tumor; Estrogen Receptor alpha; Female; Humans; MCF-7 Cells; Mice; Mice, Knockout; Protein Stability; Receptor Cross-Talk; Retinoblastoma Protein; Tumor Cells, Cultured, Estrogen Receptor alpha, Breast Neoplasms, Receptor Cross-Talk, Retinoblastoma Protein, Chaperone protein, Mice, Breast cancer, Prb, Cell Line, Tumor, MCF-7 Cells, Tumor Cells, Cultured, Estrogen receptor alpha, Animals, Humans, Female
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