信号转导子和转录激活子 5 作为正常乳腺发育生物学和乳腺癌中的关键信号通路。

Signal transducer and activator of transcription 5 as a key signaling pathway in normal mammary gland developmental biology and breast cancer.

机构信息

Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Rd NW, Research Building, Room 520A, Washington DC 20057, USA.

出版信息

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。