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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Lysophosphatidic acid enhances breast cancer cells-mediated osteoclastogenesis
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Lysophosphatidic acid enhances breast cancer cells-mediated osteoclastogenesis

机译：溶血磷脂酸增强乳腺癌细胞介导的破骨细胞生成

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pLysophosphatidic acid (LPA) is known to play a critical role in breast cancer metastasis to bone. In this study, we tried to investigate any role of LPA in the regulation of osteoclastogenic cytokines from breast cancer cells and the possibility of these secretory factors in affecting osteoclastogenesis. Effect of secreted cytokines on osteoclastogenesis was analyzed by treating conditioned media from LPA-stimulated breast cancer cells to differentiating osteoclasts. Result demonstrated that IL-8 and IL-11 expression were upregulated in LPA-treated MDA-MB-231 cells. IL-8 was induced in both MDA-MB-231 and MDA-MB-468, however, IL-11 was induced only in MDA-MB-231, suggesting differential LPARs participation in the expression of these cytokines. Expression of IL-8 but not IL-11 was suppressed by inhibitors of PI3K, NFkB, ROCK and PKC pathways. In the case of PKC activation, it was observed that PKCδ and PKCμ might regulate LPA-induced expression of IL-11 and IL-8, respectively, by using specific PKC subtype inhibitors. Finally, conditioned Medium from LPA-stimulated breast cancer cells induced osteoclastogenesis. In conclusion, LPA induced the expression of osteolytic cytokines (IL-8 and IL-11) in breast cancer cells by involving different LPA receptors. Enhanced expression of IL-8 by LPA may be via ROCK, PKCu, PI3K, and NFkB signaling pathways, while enhanced expression of IL-11 might involve PKCδ signaling pathway. LPA has the ability to enhance breast cancer cells-mediated osteoclastogenesis by inducing the secretion of cytokines such as IL-8 and IL-11.
机译：众所周知，溶血磷脂酸（LPA）在乳腺癌向骨骼的转移中起着关键作用。在这项研究中，我们试图研究LPA在调节乳腺癌细胞破骨细胞生成细胞因子中的任何作用，以及这些分泌因子影响破骨细胞生成的可能性。通过处理从LPA刺激的乳腺癌细胞中分化成破骨细胞的条件培养基，分析了分泌的细胞因子对破骨细胞形成的影响。结果表明，在LPA处理的MDA-MB-231细胞中IL-8和IL-11表达上调。 IL-8在MDA-MB-231和MDA-MB-468中均被诱导，但是IL-11仅在MDA-MB-231中被诱导，这表明LPARs参与了这些细胞因子的表达。 IL-8的表达被PI3K，NFkB，ROCK和PKC途径的抑制剂抑制。在PKC活化的情况下，观察到PKCδ和PKCμ可以通过使用特异性PKC亚型抑制剂分别调节LPA诱导的IL-11和IL-8的表达。最后，来自LPA刺激的乳腺癌细胞的条件培养基诱导破骨细胞形成。总之，LPA通过牵涉不同的LPA受体诱导乳腺癌细胞中溶骨细胞因子（IL-8和IL-11）的表达。 LPA增强IL-8的表达可能是通过ROCK，PKCu，PI3K和NFkB信号通路，而IL-11的增强表达可能涉及PKCδ信号通路。 LPA具有通过诱导细胞因子（例如IL-8和IL-11）分泌来增强乳腺癌细胞介导的破骨细胞生成的能力。

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