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从激素敏感性前列腺癌转变为激素难治性前列腺癌过程中JAK/STAT信号通路的表达水平。

Expression levels of the JAK/STAT pathway in the transition from hormone-sensitive to hormone-refractory prostate cancer.

作者信息

Tam L, McGlynn L M, Traynor P, Mukherjee R, Bartlett J M S, Edwards J

机构信息

Section of Surgical and Translational Sciences, Division of Cancer Sciences and Molecular Pathology, Glasgow Royal Infirmary, Glasgow G31 2ER, UK.

出版信息

Br J Cancer. 2007 Aug 6;97(3):378-83. doi: 10.1038/sj.bjc.6603871. Epub 2007 Jun 26.

DOI:10.1038/sj.bjc.6603871
PMID:17595657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2360337/
Abstract

The main cause of prostate cancer-related mortality is the development of hormone-refractory disease. Circulating serum levels of IL-6 are raised in hormone-refractory prostate cancer patients and evidence from cell line studies suggests that the IL-6R/JAK/STAT3 pathway may be involved in development of this disease. In the current study we investigate if expression levels of these family members are implicated in the development of hormone-refractory prostate cancer. Immunohistochemistry using IL-6R, JAK1, STAT3, pSTAT3(Tyr705) and pSTAT3(Ser727) antibodies was performed on 50 matched hormone-sensitive and hormone-refractory tumours pairs. An increase in expression of cytoplasmic IL-6 receptor, with the development of hormone-refractory prostate cancer was associated with reduced time to relapse (P=0.0074) while an increase in expression of cytoplasmic pSTAT3(Tyr705) was associated with reduced patient survival (P=0.0003). In addition, those patients with high expression of cytoplasmic pSTAT3(Tyr705) in their hormone-refractory tumours had significantly shorter time to death from biochemical relapse and overall survival in comparison to those patients with low expression of cytoplasmic pSTAT3(Tyr705) (P=0.002 and P=0.0027, respectively). Activation of STAT3, via phosphorylation is associated with reduced patient survival, suggesting that activation of the IL-6R/JAK/STAT3 pathway is involved with development of hormone-refractory prostate cancer.

摘要

前列腺癌相关死亡的主要原因是激素难治性疾病的发展。激素难治性前列腺癌患者的循环血清白细胞介素-6（IL-6）水平升高，细胞系研究证据表明IL-6受体/Janus激酶/信号转导和转录激活因子3（IL-6R/JAK/STAT3）通路可能参与了该疾病的发展。在本研究中，我们调查这些家族成员的表达水平是否与激素难治性前列腺癌的发展有关。使用IL-6R、JAK1、STAT3、磷酸化STAT3（Tyr705）和磷酸化STAT3（Ser727）抗体对50对匹配的激素敏感和激素难治性肿瘤进行免疫组织化学检测。随着激素难治性前列腺癌的发展，细胞质IL-6受体表达增加与复发时间缩短相关（P=0.0074），而细胞质磷酸化STAT3（Tyr705）表达增加与患者生存率降低相关（P=0.0003）。此外，与细胞质磷酸化STAT3（Tyr705）低表达的患者相比，激素难治性肿瘤中细胞质磷酸化STAT3（Tyr705）高表达的患者从生化复发到死亡的时间和总生存期显著缩短（分别为P=0.002和P=0.0027）。通过磷酸化激活STAT3与患者生存率降低相关，提示IL-6R/JAK/STAT3通路的激活与激素难治性前列腺癌的发展有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/130db2212018/6603871f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/1124e395ed53/6603871f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/f81faa4ff2a6/6603871f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/8f28b7ec886a/6603871f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/130db2212018/6603871f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/1124e395ed53/6603871f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/f81faa4ff2a6/6603871f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/8f28b7ec886a/6603871f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea9d/2360337/130db2212018/6603871f4.jpg

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