Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Rd NW, Research Building, Room 520A, Washington DC 20057, USA.
Breast Cancer Res. 2011 Oct 12;13(5):220. doi: 10.1186/bcr2921.
STAT5 consists of two proteins, STAT5A/B, that impact mammary cell differentiation, proliferation, and survival. In normal development, STAT5 expression and activity are regulated by prolactin signaling with JAK2/ELF5, EGF signaling networks that include c-Src, and growth hormone, insulin growth factor, estrogen, and progesterone signaling pathways. In cancer, erythropoietin signaling can also regulate STAT5. Activation levels are influenced by AKT, caveolin, PIKE-A, Pak1, c-Myb, Brk, beta-integrin, dystroglycan, other STATs, and STAT pathway molecules JAK1, Shp2, and SOCS. TGF-β and PTPN9 can downregulate prolactin- and EGF-mediated STAT5 activation, respectively. IGF, AKT, RANKL, cyclin D1, BCL6, and HSP90A lie downstream of STAT5.
STAT5 由两种蛋白组成，即 STAT5A/B，其影响乳腺细胞的分化、增殖和存活。在正常发育过程中，STAT5 的表达和活性受催乳素信号转导调控，该信号转导通过 JAK2/ELF5 与 EGF 信号网络（包括 c-Src）、生长激素、胰岛素生长因子、雌激素和孕激素信号通路相互作用。在癌症中，促红细胞生成素信号也可以调节 STAT5。激活水平受 AKT、 caveolin、PIKE-A、Pak1、c-Myb、Brk、β-整联蛋白、dystroglycan、其他 STAT 和 STAT 途径分子 JAK1、Shp2 和 SOCS 的影响。TGF-β 和 PTPN9 分别可以下调催乳素和 EGF 介导的 STAT5 激活。IGF、AKT、RANKL、cyclin D1、BCL6 和 HSP90A 位于 STAT5 的下游。
