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趋化因子配体 12/趋化因子受体 4 促进神经胶质瘤细胞的运动和增殖。

CXCL12/CXCR4 promotes motility and proliferation of glioma cells.

机构信息

Centre for Neuroscience and Cell Biology and CIMAGO, University of Coimbra, Coimbra, Portugal.

出版信息

Cancer Biol Ther. 2010 Jan;9(1):56-65. doi: 10.4161/cbt.9.1.10342. Epub 2010 Jan 17.

DOI:10.4161/cbt.9.1.10342
PMID:19923906
Abstract

Glioblastoma (GBM) is the most aggressive and malignant brain tumor. Recent studies indicated that glioma samples are characterized by increased expression of CXCR4, the CXCL12/SDF-1 chemokine receptor. To better understand the role of CXCR4 in GBM biology we performed an integrated study where we simultaneously evaluate the contribution of the CXCR4/CXCL12 signaling pathway to the proliferation, survival and motility of a human GBM cell line. Our results indicated that CXCR4/CXCL12 axis induced an increase in cell proliferation and in cell motility. The blockage of CXCR4 induced a significant increase of apoptosis. Together, our results indicated that CXCR4/CXCL12 signalling pathway may contribute to GBM development and emphasize the therapeutic potential of this pathway in patients with GBM.

摘要

胶质母细胞瘤(GBM)是最具侵袭性和恶性的脑肿瘤。最近的研究表明,神经胶质瘤样本的特征是 CXCR4(趋化因子受体 CXCL12/SDF-1)表达增加。为了更好地了解 CXCR4 在 GBM 生物学中的作用,我们进行了一项综合研究,同时评估了 CXCR4/CXCL12 信号通路对人 GBM 细胞系增殖、存活和迁移的贡献。我们的结果表明,CXCR4/CXCL12 轴诱导细胞增殖和迁移增加。CXCR4 的阻断诱导细胞凋亡显著增加。总之,我们的结果表明,CXCR4/CXCL12 信号通路可能有助于 GBM 的发展,并强调了该通路在 GBM 患者中的治疗潜力。

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