Stress hormones regulate interleukin-6 expression by human ovarian carcinoma cells through a Src-dependent mechanism
Stress hormones regulate interleukin-6 expression by human ovarian carcinoma cells through a Src-dependent mechanism
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DOI：
10.1074/jbc.m611539200
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发表时间：
2007-10-12
影响因子：
4.8
通讯作者：
Sood, Anil K.
中科院分区：
文献类型：
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作者：
Nilsson, Monique B.;Armaiz-Pena, Guillermo;Sood, Anil K.
最近的研究表明，慢性压力会促进肿瘤生长、血管生成和转移。在卵巢癌中，已知在经历慢性应激的个体中，促血管生成细胞因子白介素 6 (IL6) 的水平会升高，但该细胞因子的调节机制及其在肿瘤生长中的作用仍在研究中。在这里，我们发现去甲肾上腺素等应激激素会导致卵巢癌细胞中 IL-6 mRNA 表达和蛋白质水平增加。此外，我们证明去甲肾上腺素刺激会激活Src酪氨酸激酶，并且这种激活是增加IL-6表达所必需的。这些结果表明，应激激素激活已知对卵巢肿瘤进展至关重要的信号通路。
Recent studies have demonstrated that chronic stress promotes tumor growth, angiogenesis, and metastasis. In ovarian cancer, levels of the pro- angiogenic cytokine, interleukin 6 ( IL6), are known to be elevated in individuals experiencing chronic stress, but the mechanism( s) by which this cytokine is regulated and its role in tumor growth remain under investigation. Here we show that stress hormones such as norepinephrine lead to increased expression of IL- 6mRNAand protein levels in ovarian carcinoma cells. Furthermore, we demonstrate that norepinephrine stimulation activates Src tyrosine kinase and this activation is required for increased IL- 6 expression. These results demonstrate that stress hormones activate signaling pathways known to be critical in ovarian tumor progression.