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  • 标题:JNK and PTEN cooperatively control the development of invasive adenocarcinoma of the prostate
  • 本地全文:下载
  • 作者:Anette Hübner ; David J. Mulholland ; Claire L. Standen
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:2012
  • 卷号:109
  • 期号:30
  • 页码:12046-12051
  • DOI:10.1073/pnas.1209660109
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:The c-Jun NH2-terminal kinase (JNK) signal transduction pathway is implicated in cancer, but the role of JNK in tumorigenesis is poorly understood. Here, we demonstrate that the JNK signaling pathway reduces the development of invasive adenocarcinoma in the phosphatase and tensin homolog (Pten) conditional deletion model of prostate cancer. Mice with JNK deficiency in the prostate epithelium ({Delta}Jnk {Delta}Pten mice) develop androgen-independent metastatic prostate cancer more rapidly than control ({Delta}Pten) mice. Similarly, prevention of JNK activation in the prostate epithelium ({Delta}Mkk4 {Delta}Mkk7 {Delta}Pten mice) causes rapid development of invasive adenocarcinoma. We found that JNK signaling defects cause an androgen-independent expansion of the immature progenitor cell population in the primary tumor. The JNK-deficient progenitor cells display increased proliferation and tumorigenic potential compared with progenitor cells from control prostate tumors. These data demonstrate that the JNK and PTEN signaling pathways can cooperate to regulate the progression of prostate neoplasia to invasive adenocarcinoma.
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