Kimbro K Sean, Duschene Kaitlin, Willard Margeret, Moore Jodi-Ann, Freeman Shalonda
Department of Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA.
Mol Biol Rep. 2008 Mar;35(1):23-7. doi: 10.1007/s11033-006-9047-1. Epub 2007 Apr 6.
The human STYK1/NOK protein is approximately 30-35% similar to mouse fibroblast growth factor receptor 3 and a kinase homologue in D. melanogaster in the tyrosine protein kinase region. STYK1/NOK was identified as being up regulated in MDA-MB-231, an estrogen receptor-alpha negative breast cancer cell line, following 12 h of estrogen treatment at 1x10(-9) M. On further investigation of STYK1/NOK in estrogen treated cell line MDA-MB-231, STYK1/NOK was up regulated at 6 h post treatment when compared to untreated cells. We also investigated the expression levels of STYK1/NOK in other breast cancer cell lines MCF-7, MDA-MB-231, BT-549, and MDA-MB-435S using QRT-PCR. In addition, the analysis of message accumulation was increased with other synthetic estrogen response modifiers. We propose that the regulation of STYK1/NOK is achieved independent of ERalpha and suggests further investigation to the relevance of this kinase in breast cancer progression.
人类STYK1/NOK蛋白在酪氨酸蛋白激酶区域与小鼠成纤维细胞生长因子受体3以及黑腹果蝇中的一种激酶同源物大约有30%-35%的相似性。在1×10(-9)M雌激素处理12小时后,STYK1/NOK在雌激素受体α阴性的乳腺癌细胞系MDA-MB-231中被鉴定为上调。在对雌激素处理的细胞系MDA-MB-231中的STYK1/NOK进行进一步研究时,与未处理的细胞相比,STYK1/NOK在处理后6小时上调。我们还使用定量逆转录聚合酶链反应(QRT-PCR)研究了STYK1/NOK在其他乳腺癌细胞系MCF-7、MDA-MB-231、BT-549和MDA-MB-435S中的表达水平。此外,其他合成雌激素反应调节剂会增加信息积累的分析。我们提出STYK1/NOK的调节是独立于雌激素受体α实现的,并建议进一步研究这种激酶在乳腺癌进展中的相关性。