Normal and Cancer-Related Functions of the p160 Steroid Receptor Coactivator (SRC) Family

Extracellular signals and their signaling pathways cause posttranslational modifications of SRCs, which regulate the cellular concentrations, activities and specificities of SRCs. In general, SRCs enhance steroid receptor functions and facilitate hormonal promotion of breast, prostate and ovarian cancers. Specifically, SRC-1 enhances Ets-2-mediated HER2 expression and PEA3-mediated Twist expression and upregulates CSF-1 expression to promote breast tumor cell migration, invasion and metastasis. MOZ and SRC-2 fusion gene causes AML (acute myeloid leukemia). SRC-3 upregulates its own expression through serving as a coactivator for E2F1 and SP1. The overexpressed SRC-3 enhances PEA3 and AP-1 mediated MMP expression to promote breast and prostate tumor cell metastasis. SRC-3 also enhances E2F1-mediated cell cycle progression and Gab2 expression that activates Akt. In addition, SRC-3 upregulates IGF-I, IRS-1 and IRS-2 to promote the IGF-I signaling pathway and to activate EGFR and ERBB2 to enhance Akt and MAPK activities, resulting in hyperactivation of Akt and MAPK which contribute to cancer cell proliferation, growth, survival, migration, invasion and metastasis.

Publication

Normal and Cancer-Related Functions of the p160 Steroid Receptor Coactivator (SRC) Family. () Jianming Xu, et al. Nat Rev Cancer. ;9(9):615-630. Figure: F3. All organisms Homo sapiens Mus musculus Drosophila melanogaster

Disease mentions