Quantification of PRL/Stat5 signaling with a novel pGL4-CISH reporter.
Quantification of PRL/Stat5 signaling with a novel pGL4-CISH reporter.
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DOI：
10.1186/1472-6750-8-11
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发表时间：
2008-02-06
影响因子：
3.5
通讯作者：
Clevenger CV
中科院分区：
文献类型：
--
作者：
Fang F;Antico G;Zheng J;Clevenger CV
血清催乳素 (PRL) 升高与乳腺癌风险增加相关。 PRL 信号传导通过其催乳素受体 (PRLr) 涉及 Jak2/Stat5 途径。基于荧光素酶的报告基因检测已被广泛用于评估该途径的活性。然而，现有的报告基因往往不够灵敏，无法监测 PRL 在此途径中的作用。在本研究中，产生了一种新的生物学相关报告基因 pGL4-CISH，用于研究 PRL/Jak2/Stat5 信号通路。 pGL4-CISH 检测 PRL 的灵敏度优于其他几种常用的 Stat5 响应报告基因。有趣的是，增强功能的pGL4-CISH仅限于雌激素受体阳性（ER+）人乳腺癌细胞系T47D和MCF7，但不在ER-MDA-231、BT-474或MCF10A细胞系中。 Stat5 的过表达进一步增强了 PRL 对 pGL4-CISH 的作用。这些研究表明，pGL4-CISH 是一种新颖且灵敏的报告基因，可用于评估 ER+ 人乳腺癌细胞中 PRL/Stat5 信号通路的活性。
Elevations of serum prolactin (PRL) are associated with an increased risk for breast cancer. PRL signaling through its prolactin receptor (PRLr) involves the Jak2/Stat5 pathway. Luciferase-based reporter assays have been widely used to evaluate the activity of this pathway. However, the existing reporters are often not sensitive enough to monitor the effect of PRL in this pathway. In this study, a new biologically relevant reporter, pGL4-CISH, was generated to study the PRL/Jak2/Stat5 signaling pathway. The sensitivity of pGL4-CISH to detect PRL was superior to that of several other commonly utilized Stat5-responsive reporters. Interestingly, the enhanced function pGL4-CISH was restricted to the estrogen receptor positive (ER+) human breast cancer cell lines T47D and MCF7, but not in the ER-MDA-231, BT-474, or MCF10A cell lines. Overexpression of Stat5 further enhanced the effect of PRL on pGL4-CISH. These studies demonstrate that pGL4-CISH is a novel and sensitive reporter for assessing the activity of the PRL/Stat5 signaling pathway in the ER+ human breast cancer cells.
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影响因子：
64.5
作者：
Parganas, E;Wang, D;Ihle, JN
通讯作者：
Ihle, JN
影响因子：
8
作者：
Miller, S. L.;Antico, G.;Clevenger, C. V.
通讯作者：
Clevenger, C. V.
影响因子：
14.9
作者：
Voon, DC;Subrata, LS;Daly, JM
通讯作者：
Daly, JM
影响因子：
11.4
作者：
GOUILLEUX, F;WAKAO, H;GRONER, B
通讯作者：
GRONER, B
影响因子：
4.8
作者：
Dif, F;Saunier, E;Edery, M
通讯作者：
Edery, M