Department of Dermatology and IZKF Münster, University of Münster, Münster, Germany.
J Invest Dermatol. 2012 Feb;132(2):375-84. doi: 10.1038/jid.2011.314. Epub 2011 Oct 13.
Recent studies have indicated an important role of proteinases and proteinase-activated receptors (PARs) in tumorigenesis. Although a role for PARs has been described in various skin tumors including melanoma, the underlying cellular mechanisms have not been understood. Recent studies have suggested PAR(1) as a regulator of melanoma cell growth and metastasis by affecting angiogenic and invasive factors. Moreover, changes in the expression patterns of PAR(1) and PAR(2) correlate with skin cancer progression, and PAR(1) is overexpressed in melanoma. Therefore, we sought to elucidate the putative role of PAR(1)- and PAR(2)-mediated signal transduction pathways during melanoma progression. Activation of both PAR(1) and PAR(2) led to rapid phosphorylation of protein kinase D1 (PKD1) in cultured WM9 melanoma cells. PKD1 is known to be involved in cell migration, integrin regulation, and intracellular vesicle transport. Downregulation of PKD1 by siRNA resulted in diminished proliferation, decreased αvβ3 integrin regulation, and secretion of pro-angiogenic chemokine IL-8 in WM9 cells. In conclusion, our results show that PAR(1) and PAR(2) are involved in WM9 cell proliferation and secretion of IL-8 by activation of PKD1. Inactivation of the PKD1 pathway may be beneficial for the inhibition of PAR-induced melanoma proliferation and for maintenance of the inflammatory tumor environment.
最近的研究表明蛋白酶和蛋白酶激活受体(PARs)在肿瘤发生中起着重要作用。虽然 PARs 在各种皮肤肿瘤中,包括黑色素瘤,已经被描述了其作用,但其潜在的细胞机制尚不清楚。最近的研究表明,PAR(1)通过影响血管生成和侵袭因子来调节黑色素瘤细胞的生长和转移。此外,PAR(1)和 PAR(2)的表达模式的变化与皮肤癌的进展相关,并且 PAR(1)在黑色素瘤中过表达。因此,我们试图阐明 PAR(1)和 PAR(2)介导的信号转导通路在黑色素瘤进展中的潜在作用。在培养的 WM9 黑色素瘤细胞中,PAR(1)和 PAR(2)的激活均导致蛋白激酶 D1(PKD1)的快速磷酸化。PKD1 已知参与细胞迁移、整合素调节和细胞内囊泡运输。siRNA 下调 PKD1 导致 WM9 细胞增殖减少、αvβ3 整合素调节减少以及促血管生成趋化因子 IL-8 的分泌减少。总之,我们的结果表明,PAR(1)和 PAR(2)通过激活 PKD1 参与 WM9 细胞的增殖和 IL-8 的分泌。PKD1 通路的失活可能有益于抑制 PAR 诱导的黑色素瘤增殖和维持炎症性肿瘤环境。