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- Be066bc49f6f3e3e2c22c6c4c6edf4227 NCIT_P378 "BIOCARTA" @default.
- Be066bc49f6f3e3e2c22c6c4c6edf4227 type Axiom @default.
- Be066bc49f6f3e3e2c22c6c4c6edf4227 annotatedProperty NCIT_P325 @default.
- Be066bc49f6f3e3e2c22c6c4c6edf4227 annotatedSource NCIT_C39158 @default.
- Be066bc49f6f3e3e2c22c6c4c6edf4227 annotatedTarget "Approximately 30% of breast carcinomas lack ER expression. Presumably, these breast cancers become estrogen independent through genetic alterations that bypass the requirement for ER-dependent stimulation of cell proliferation. As such, estrogen receptor is a key regulator of proliferation and differentiation in mammary epithelia and represents a crucial prognostic indicator and therapeutic target in breast cancer. Mechanistically, estrogen receptor induces changes in gene expression through direct gene activation of a number of genes (e.g., cathepsin D, HSP27, alpha-tubulin, glyceraldehyde-3-phosphatase, Pdzk1, Greb) and also through the biological functions of target loci. The product of human MTA3 has been identified as an estrogen-dependent component of the Mi-2/NuRD transcriptional corepressor in breast epithelial cells and demonstrates that MTA3 constitutes a key component of an estrogen-dependent pathway regulating growth and differentiation. The absence of estrogen receptor or of MTA3 leads to aberrant expression of the transcriptional repressor Snail, a master regulator of epithelial to mesenchymal transitions. Aberrant Snail expression results in loss of expression of the cell adhesion molecule E-cadherin, an event associated with changes in epithelial architecture and invasive growth. MTA3 is the mechanistic link between estrogen receptor status and invasive growth of breast cancers. (This definition may be outdated - see the DesignNote.)" @default.