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首页> 外文期刊>Biochemical and Biophysical Research Communications >Apolipoprotein M promotes proliferation and invasion in non-small cell lung cancers via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways
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Apolipoprotein M promotes proliferation and invasion in non-small cell lung cancers via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways

机译:载脂蛋白M通过上调S1PR1促进非小细胞肺癌中的增殖和侵袭,并激活ERK1 / 2和PI3K / AKT信号传导途径

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摘要

Apolipoprotein M (ApoM) is a sphingosine 1-phosphate (SIP) carrier involved in the regulation of SIR. Signaling pathways involving sphingosine kinases (SphKs) and SIP-SIP receptors (S1PRs) play important roles in the oncogenesis of multiple cancers including non-small cell lung cancer (NSCLC). In the present study we have clarified the potential roles of ApoM on the oncogenesis process of NSCLC cells. We detected the ApoM expression in NSCLC tissues and further analyzed its clinical significance. Moreover, we determined effects of ApoM overexpression on tumor cellular behaviours of NSCLC in vitro and in vivo. Our results demonstrated that ApoM protein mass were clearly higher in the NSCLC tissues than in non-NSCLS tissues. Overexpression of ApoM could promote NSCLC cell proliferation and invasion in vitro and tumor growth in vivo, which might be via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways. It is concluded that up-regulation of ApoM in NSCLC might be associated with the tumor induced inflammation and tumor microenvironment as well as promoting oncogenesis of NSCLC. Further study needs to elucidate the underlying mechanisms. (C) 2018 Elsevier Inc. All rights reserved.
机译:载脂蛋白M(APOM)是参与SIR调节的鞘氨酸1-磷酸酯(SIP)载体。涉及鞘氨醇激酶(SPHK)和SIP-SIP受体(S1PRS)的信号传导途径在包括非小细胞肺癌(NSCLC)的多种癌症的血管生成中起重要作用。在本研究中,我们阐明了APOM对NSCLC细胞的肿瘤发生过程的潜在作用。我们在NSCLC组织中检测到APOM表达,并进一步分析其临床意义。此外,我们确定了APOM过表达对体外和体内NSCLC肿瘤细胞行为的影响。我们的结果表明,NSCLC组织中的APOM蛋白质质量明显高于非NSCLS组织。 APOM的过度表达可以促进体内的NSCLC细胞增殖和侵袭体内的侵袭,这可能是通过上调S1PR1并激活ERK1 / 2和PI3K / AKT信号传导途径。得出结论,NSCLC中APOM的上调可能与肿瘤诱导的炎症和肿瘤微环境相关,以及促进NSCLC的血管生成。进一步的研究需要阐明潜在的机制。 (c)2018年Elsevier Inc.保留所有权利。

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