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陈秋丹, 陈淑英. 胶质瘤组织中miR-218的表达及其对血管生成的作用[J]. 肿瘤防治研究, 2019, 46(8): 672-676. DOI: 10.3971/j.issn.1000-8578.2019.18.2017
引用本文: 陈秋丹, 陈淑英. 胶质瘤组织中miR-218的表达及其对血管生成的作用[J]. 肿瘤防治研究, 2019, 46(8): 672-676. DOI: 10.3971/j.issn.1000-8578.2019.18.2017
CHEN Qiudan, CHEN Shuying. MiR-218 Expression in Glioma Tissues and Its Effect on Angiogenesis[J]. Cancer Research on Prevention and Treatment, 2019, 46(8): 672-676. DOI: 10.3971/j.issn.1000-8578.2019.18.2017
Citation: CHEN Qiudan, CHEN Shuying. MiR-218 Expression in Glioma Tissues and Its Effect on Angiogenesis[J]. Cancer Research on Prevention and Treatment, 2019, 46(8): 672-676. DOI: 10.3971/j.issn.1000-8578.2019.18.2017

胶质瘤组织中miR-218的表达及其对血管生成的作用

MiR-218 Expression in Glioma Tissues and Its Effect on Angiogenesis

  • 摘要:
    目的 明确miR-218在胶质瘤组织中的表达,探讨其对胶质瘤血管生成的作用及机制。
    方法 采用荧光实时定量PCR法和免疫印迹法检测胶质瘤组织和细胞中miR-218、P70核糖体S6激酶1(p70s6k1)的表达情况,采用基质胶塞实验和小管形成实验分别在体内外检测miR-218对新血管生成的影响。
    结果 21例胶质瘤组织标本中miR-218表达较7例癌旁组织标本明显下调,且表达量与WHO分级有关。过表达miR-218能显著抑制血管生成。MiR-218直接靶向p70s6k1。过表达p70s6k1能部分逆转miR-218对血管新生的抑制作用。
    结论 MiR-218能通过靶向p70s6k1的表达调控胶质瘤血管生成,进而影响胶质瘤的进展。

     

    Abstract:
    Objective To explore the expression of miR-218 in glioma tissues, and investigate the function and mechanism of miR-218 in regulating glioma angiogenesis.
    Methods qRT-PCR and Western blot were used to detect the expression of miR-218 and p70s6k1 in glioma tissues and cells. Matrigel plug assay and tube formation assay were performed to explore tumor angiogenesis in vitro and in vivo.
    Results The expressions of miR-218 in 21 cases of glioma tissues were decreased, compared with 7 cases of normal brain tissues, and the levels were related with the WHO grade of glioma. Overexpression of miR-218 could significantly inhibit glioma angiogenesis in vitro and in vivo. MiR-218 could directly target p70s6k1. Overexpression of p70s6k1 could partially reverse the inhibition effect of miR-218 on glioma angiogenesis.
    Conclusion MiR-218 could affect the progression of glioma through regulating glioma angiogenesis by directly targeting p70s6k1 expression.

     

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