Glucosamine inhibits IL-1β-mediated IL-8 production in prostate cancer cells by MAPK attenuation

Cheng Yen Tsai, Tzong Shyuan Lee, Yu Ru Kou, Yuh Lin Wu*

*此作品的通信作者

研究成果: Article同行評審

29 引文 斯高帕斯(Scopus)

摘要

Inflammation is a complex process involving cytokine production to regulate host defense cascades. In contrast to the therapeutic significance of acute inflammation, a pathogenic impact of chronic inflammation on cancer development has been proposed. Upregulation of inflammatory cytokines, such as IL-1β and IL-8, has been noted in prostate cancer patients and IL-8 has been shown to promote prostate cancer cell proliferation and migration; however, it is not clear whether IL-1β regulates IL-8 expression in prostate cancer cells. Glucosamine is widely regarded as an anti-inflammatory agent and thus we hypothesized that if IL-1β activated IL-8 production in prostate cancer cells, then glucosamine ought to blunt such an effect. Three prostate cancer cell lines, DU-145, PC-3, and LNCaP, were used to evaluate the effects of IL-1β and glucosamine on IL-8 expression using ELISA and RT-PCR analyses. IL-1β elevated IL-8 mRNA expression and subsequent IL-8 secretion. Glucosamine significantly inhibited IL-1β-induced IL-8 secretion. IL-8 appeared to induce LNCaP cell proliferation by MTT assay; involvement of IL-8 in IL-1β-dependent PC-3 cell migration was demonstrated by wound-healing and transwell migration assays. Inhibitors of MAPKs and NFκB were used to pinpoint MAPKs but not NFκB being involved in IL-1β-mediated IL-8 production. IL-1β-provoked phosphorylation of all MAPKs was notably suppressed by glucosamine. We suggest that IL-1β can activate the MAPK pathways resulting in an induction of IL-8 production, which promotes prostate cancer cell proliferation and migration. In this context, glucosamine appears to inhibit IL-1β-mediated activation of MAPKs and therefore reduces IL-8 production; this, in turn, attenuates cell proliferation/migration.

原文English
頁(從 - 到)489-498
頁數10
期刊Journal of Cellular Biochemistry
108
發行號2
DOIs
出版狀態Published - 1 10月 2009

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