儿童星形细胞瘤、室管膜瘤和原始神经外胚层肿瘤中的白细胞介素-1α(IL-1α)、IL-1β、I型IL-1受体、IL-1受体拮抗剂和TGFβ1 mRNA。

S E Ilyin, I González-Gómez, F H Gilles, C R Plata-Salamán
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引用次数: 19

摘要

白细胞介素-1 α (IL-1 α)、IL-1 β、白细胞介素-1受体I型(IL-1RI,信号受体)和IL-1受体拮抗剂(IL-1Ra,内源性抑制剂)是IL-1系统的关键组成部分。IL-1及由IL-1诱导的其他细胞因子,如tgf - β 1,可能参与多种肿瘤细胞的生长。在儿童中,原发性神经系统肿瘤是最常见的实体恶性肿瘤。我们使用敏感和特异性的RNase保护试验研究了儿童星形细胞瘤(n = 19)、室管膜瘤(n = 13)和原始神经外表皮肿瘤(n = 22)中IL-1 α、IL-1 β、IL-1RI、IL-1Ra和tgf - β 1 mrna的水平。数据显示不同脑肿瘤类型的细胞因子mRNA谱有显著差异。毛细胞、非毛细胞和间变性星形细胞瘤的IL-1 β、IL-1RI和tgf - β 1 mRNA水平显著升高,但IL-1Ra mRNA水平较低;这可能与星形细胞瘤中IL-1 β反馈系统和IL-1 β - tgf - β 1相互作用有关。室管膜瘤显示IL-1 α和IL-1 β mRNA水平升高,而IL-1Ra mRNA水平较低;原始神经外胚层肿瘤没有表现出任何细胞因子成分水平的增加。这些数据还表明,刺激和抑制细胞因子之间平衡的失调可能通过自分泌/旁分泌机制参与脑肿瘤的生长和发展。
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Interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-1 receptor type I, IL-1 receptor antagonist, and TGF-beta 1 mRNAs in pediatric astrocytomas, ependymomas, and primitive neuroectodermal tumors.

Interleukin-1 alpha (IL-1 alpha), IL-1 beta, interleukin-1 receptor type I (IL-1RI, signaling receptor), and IL-1 receptor antagonist (IL-1Ra, endogenous inhibitor) are pivotal components of the IL-1 system. IL-1 and other cytokines induced by IL-1, such as TGF-beta 1, may participate in the growth of various tumor cells. In children, primary nervous system tumors represent the most common solid malignancy. We investigated the levels of IL-1 alpha, IL-1 beta, IL-1RI, IL-1Ra, and TGF-beta 1 mRNAs in pediatric astrocytomas (n = 19), ependymomas (n = 13), and primitive neuroectodermal tumors (n = 22) using sensitive and specific RNase protection assays. The data show a significant distinct cytokine mRNA profile among brain tumor types. Pilocytic, nonpilocytic, and anaplastic astrocytomas have significant increased levels of IL-1 beta, IL-1RI, and TGF-beta 1 mRNAs, but low levels of IL-1Ra mRNA; this may have implications for an IL-1 beta feedback system and IL-1 beta<-->TGF-beta 1 interactions in astrocytomas. Ependymomas show increased levels of IL-1 alpha and IL-1 beta mRNAs associated with low levels of IL-1Ra mRNA; primitive neuroectodermal tumors do not exhibit increased levels of any cytokine component examined. The data also suggest that a dysregulation of the balance between stimulatory and inhibitory cytokines may be involved in the growth and development of brain tumors via autocrine/paracrine mechanisms.

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