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miR-92a 是胶质母细胞瘤中凋亡途径的关键调节因子,与 BCL2L11 的表达呈负相关。

miR-92a is a critical regulator of the apoptosis pathway in glioblastoma with inverse expression of BCL2L11.

机构信息

Department of Neurosurgery, Sir Run Run Shaw Hospital, Medical College, Zhejiang University, Hangzhou 310016, PR China.

出版信息

Oncol Rep. 2012 Nov;28(5):1771-7. doi: 10.3892/or.2012.1970. Epub 2012 Aug 10.

DOI:10.3892/or.2012.1970
PMID:22895567
Abstract

Recent studies have revealed that miR-92a is overexpressed in several types of malignancies and provides a protumorigenic effect. Our findings demonstrate that the high expression of miR-92a in human glioma specimens is significantly correlated with low levels of BCL2L11 (Bim) protein and high-grade glioma. Here, we present the first evidence that miR-92a antisense oligonucleotide (AS-miR-92a) provides a tumor suppressive effect via induction of apoptosis in human glioma cells. In addition, we show that Bim is a direct functional target of miR-92a. Introducing Bim cDNA without 3'UTR abrogates miR-92a-induced cell survival. Further investigations will focus on the therapeutic use of AS-miR‑92a-mediated antitumor effects in glioma.

摘要

最近的研究表明,miR-92a 在几种类型的恶性肿瘤中过表达,并具有促进肿瘤发生的作用。我们的研究结果表明,miR-92a 在人胶质瘤标本中的高表达与 BCL2L11(Bim)蛋白水平降低和高级别胶质瘤显著相关。在这里,我们首次提供证据表明,miR-92a 反义寡核苷酸(AS-miR-92a)通过诱导人胶质瘤细胞凋亡发挥肿瘤抑制作用。此外,我们表明 Bim 是 miR-92a 的直接功能靶标。引入没有 3'UTR 的 Bim cDNA 可消除 miR-92a 诱导的细胞存活。进一步的研究将集中于 AS-miR-92a 在胶质瘤中的抗肿瘤作用的治疗用途。

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