IL-8通过激活PKC/ERK信号通路促进肾癌细胞上皮细胞-间质细胞转化
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国家自然科学基金资助项目(81101519),广东省自然科学基金资助项目(S2011040003777).


IL-8 Regulates The Epithelial-mesenchymal Transition (EMT) of Renal Cancer Through PKC/ERK Signaling Pathway
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This work was supported by grants from The National Natural Science Foundation of China (81101519), The Natural Science Foundation of Guangdong (S2011040003777)

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    摘要:

    上皮细胞-间质细胞转化(EMT)在肿瘤转移方面起着非常重要的作用.肾癌发生EMT的具体分子机制尚不清楚.IL-8是一个重要的炎症趋化因子,研究表明肾癌细胞可以分泌IL-8,但IL-8是否参与肾癌细胞EMT的调节目前尚无报道.我们研究发现,IL-8可以促进肾癌细胞形态发生间质化改变,IL-8刺激后E-钙黏蛋白表达水平下降, N-钙黏蛋白表达上调.另外,IL-8可以促进肾癌细胞侵袭,但对肾癌细胞增殖的影响并不明显.进一步研究显示,IL-8通过激活蛋白激酶C(PKC)引起细胞外调节性激酶(ERK)磷酸化.因此,我们认为IL-8可能通过PKC/ERK信号通路促进肾癌细胞发生EMT,这可能是肾癌转移的重要机制之一.

    Abstract:

    The epithelial-mesenchymal transition (EMT) is an essential component in tumor metastasis. However, the molecular mechanism of EMT in renal cancer is unclear. IL-8 is an important chemokine in tumor microenvironment. Studies have shown that renal cancer cells can secrete IL-8,whether it could induce EMT in renal cancer cells is unknown. Here we found that IL-8 could induce EMT in renal cancer cells. Upon the stimulation of IL-8,the expression of E-cadherin was up-regulated,while the expression of N-cadherin was down-regulated; IL-8 promoted the invasion of renal cancer cells, but there was no obvious impact on cell proliferation. In addition, IL-8 could activate ERK through PKC. Therefore, we believe that IL-8 may promote renal cancer EMT through PKC / ERK signaling pathway, which may be one of the important mechanisms of renal cancer metastasis.

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毕良宽,林天歆,许可慰,韩金利,黄 海,张彩霞,董 文,刘 皓,黄健. IL-8通过激活PKC/ERK信号通路促进肾癌细胞上皮细胞-间质细胞转化[J].生物化学与生物物理进展,2012,39(10):981-986

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  • 收稿日期:2012-06-14
  • 最后修改日期:2012-09-07
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  • 在线发布日期: 2012-09-14
  • 出版日期: 2012-10-20