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上皮样肉瘤中以微囊泡形式释放的外泌体蛋白,与成纤维细胞相互作用。

Emmprin, released as a microvesicle in epithelioid sarcoma, interacts with fibroblasts.

机构信息

Department of Pathology, Fukuoka University Hospital and School of Medicine, Fukuoka, Japan.

Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.

出版信息

Int J Oncol. 2017 Jun;50(6):2229-2235. doi: 10.3892/ijo.2017.3986. Epub 2017 May 8.

Abstract

Emmprin (extracellular matrix metalloproteinase inducer, CD147) is a glycosylated transmembrane protein, consisting of two immunoglobulin domains, that stimulates the production of matrix metalloproteinases (MMPs) by tumor-associated fibroblasts. These effects play important roles in tumor invasion and metastasis. However, the precise mechanisms by which emmprin acts on fibroblasts have not been fully elucidated, especially in sarcoma cells. Previously, we demonstrated that emmprin, expressed in conditioned medium collected from the epithelioid sarcoma cell line (FU-EPS-1), stimulates MMP-2 production via interactions with fibroblasts. In this study, we used microvesicles derived from sarcoma cells, and determined whether emmprin exists in the microvesicles, which enhance the production of MMP-2 via fibroblasts. Microvesicles released from FU-EPS-1 cells were shown to contain full-length emmprin, identified as a 45-kDa protein characterized by polylactosamine glycosylation. Microvesicles collected from FU-EPS-1 cells transfected with emmprin-specific siRNA or transduced with shRNA displayed significantly reduced MMP-2 production by fibroblasts compared with those from control-transfected cells. Our findings show that emmprin is released through microvesicle shedding in sarcoma cells, and emmprin in microvesicles regulates MMP-2 production by influencing the activity of fibroblasts located at sites distant from the tumor cells.

摘要

上皮样肉瘤细胞来源的微囊泡通过 emmprin 诱导成纤维细胞产生 MMP-2

外泌型基质金属蛋白酶诱导因子(extracellular matrix metalloproteinase inducer,CD147)是一种糖基化跨膜蛋白,由两个免疫球蛋白结构域组成,可刺激肿瘤相关成纤维细胞产生基质金属蛋白酶(matrix metalloproteinases,MMPs)。这些作用在肿瘤侵袭和转移中发挥着重要作用。然而,emmprin 作用于成纤维细胞的确切机制尚未完全阐明,特别是在肉瘤细胞中。此前,我们证明了表达在上皮样肉瘤细胞系(FU-EPS-1)条件培养基中的 emmprin 通过与成纤维细胞相互作用刺激 MMP-2 的产生。在这项研究中,我们使用了来源于肉瘤细胞的微囊泡,并确定了 emmprin 是否存在于增强 MMP-2 产生的微囊泡中。结果显示,FU-EPS-1 细胞释放的微囊泡中含有全长的 emmprin,被鉴定为 45kDa 的蛋白,具有多乳糖胺糖基化的特征。与对照转染细胞相比,转染了 emmprin 特异性 siRNA 的 FU-EPS-1 细胞或转导了 shRNA 的 FU-EPS-1 细胞收集的微囊泡导致成纤维细胞产生的 MMP-2 显著减少。我们的研究结果表明,emmprin 通过肉瘤细胞的微囊泡脱落释放,并且微囊泡中的 emmprin 通过影响位于远离肿瘤细胞部位的成纤维细胞的活性来调节 MMP-2 的产生。

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