aPKC lambda/iota promotes growth of prostate cancer cells in an autocrine manner through transcriptional activation of interleukin-6 (PNAS, 2009, 106:16369-16374)

報告日期: 2010/10/08
報告時間: 17:10/18:00
報告學生: 侯雅琴
講評老師: 凌 斌

Full Text: http://basicmed.med.ncku.edu.tw/admin/up_img/991008-2.pdf

aPKCλ/ι promotes growth of prostate cancer cells in an autocrine manner through transcriptional activation of interleukin-6

Hitoshi Ishiguro, Kazunori Akimoto, Yoji Nagashima, Yasuyuki Kojima, Takeshi Sasaki, Yukari Ishiguro-Imagawa, Noboru Nakaigawa, Shigeo Ohno, Yoshinobu Kubota, and Hiroji Uemura

PNAS, 2009, 106:16369-16374



Commentator凌斌 老師

Date2010.10.08  PM16:10-17:00

PlaceRoom 602



Prostate cancer is the second leading cause of cancer deaths in men in western countries and currently ranks the 7th mortality rate in Taiwan. Hormone ablation so far remains the first-line treatment of prostate cancer. But hormone ablation therapy eventually fails for the most patients due to the diseases developing into hormone refractory pros­tate cancer (HRPC). Alterations in HRPC include androgen receptor (AR) changes. In addition, the AR is activated by cytokines such as interleukin-6 (IL-6). There are several reports showing the importance of IL-6 in prostate cancer progression, the mechanism by which IL-6 expression is regulated in prostate cancer cells is not fully understood. Atypical protein kinase C (aPKCλ/ι) has been implicated in the progression of several cancers. Recent studies suggest that enhanced aPKC expression in human prostate cancer tissues, but the relationship between aPKCλ/ι and prostate cancer progression remains unclear. In this study, the authors show evidence that aPKCλ/ι expression correlates with prostate cancer recurrence. Experiments in vitro and in vivo revealed aPKCλ/ι to be involved in prostate cancer cell growth through secretion of IL-6. Further, aPKCλ/ι activates transcription of the IL-6 gene through NF-κB and AP-1. These results emphasizes that aPKCλ/ι promotes the growth of hormone indepen­dent prostate cancer cells by stimulating IL-6 production in an autocrine manner. These findings not only explain the link between aPKCλ/ι and IL-6, but also establish a molecular change involved in the development of HRPC.



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