MiR-561通过C-myc调控抑制胶质母细胞瘤细胞增殖

IF 0.4 Q4 ONCOLOGY
S. Karami, F. Kouhkan, Iman Rad, Nafiseh Tavakolpoor Saleh, Gelareh Shokri, P. Fallah, M. Hashemi
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引用次数: 1

摘要

背景:多形性胶质母细胞瘤(GBM)是成人最常见的原发性恶性脑肿瘤。miRNA表达的调节既被认为是癌症发展和侵袭的控制基础,也被认为是gbm靶向治疗的潜在应用,无论是单独治疗还是联合化疗或放疗。c-myc过表达与GBM进展性生长和恶性肿瘤密切相关。有充分的证据表明,microRNAs (miRNAs)与几种恶性肿瘤的发病机制有关。然而,关于mirna在GBM发展中的潜在作用知之甚少。我们进行本研究是为了了解miR-561是否通过控制c-myc的表达来抑制GBM细胞的增殖和存活。方法:在体外研究中,以U87细胞系为模板构建慢病毒载体“pCDH-miR-561”。用pCDH-miR-561转染HEK293细胞株,检测其活力(MTT法)和凋亡率(流式细胞术)。采用q-RT PCR检测c-myc的表达。为了寻找可能的miR-561p靶点,我们使用了TargetScan和DAVID的生物信息学工具。结果:我们的研究结果证实了miR-561在GBM癌细胞中过表达抑制细胞增殖,促进细胞凋亡,这与c-myc的下调密切相关。结论:这些发现表明miR-561具有通过调节c-myc抑制U87生长和增殖的良好条件,从而使其成为GBM治疗的有用模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The MiR-561 Suppresses Glioblastoma Cell Proliferation through C-myc Regulation
Background: Glioblastoma multiforme (GBM) is the most common primary malignat brain tumor in adults. The modulation of miRNA expression is taken into consideration both as controlling groundwork for cancer development and invasion and as a potential application in GBM-targeted therapies either perse or combined with chemo or radiotherapy. The c-myc overexpression is tightly correlated with GBM progressing growth and malignancy. There is ample evidence showing that microRNAs (miRNAs) are linked to the pathogenesis of several malignancies. However, little is known about the potential role of miRNAs in GBM development. We conducted the present study to find out whether the miR-561 inhibits GBM cells proliferation and survival via controlling the expression of c-myc. Method: In this in vitro study, the U87 cell line was used as a template for lentiviral vector “pCDH-miR-561” construction. HEK293 cell line was transfected with pCDH-miR-561 and its viability (MTT assay) and apoptosis rates (flow cytometry) were monitored. c-myc expression was monitored employing q-RT PCR. In order to search for possible miR-561p targets, we utilized bioinformatics tools of TargetScan and DAVID. Results: Our results confirmed that the overexpression of the miR-561 inhibits cell proliferation and promotes cell apoptosis in GBM cancer cells, which is tightly correlated with the downregulation of c-myc. Conclusion: These findings proposed that the miR-561 has promising qualifications to suppress U87 growth and proliferation via tuning the c-myc, which then makes it a useful model for GBM treatment.
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来源期刊
CiteScore
0.80
自引率
0.00%
发文量
0
审稿时长
12 weeks
期刊介绍: Middle East Journal of Cancer (MEJC) is an international peer-reviewed journal which aims to publish high-quality basic science and clinical research in the field of cancer. This journal will also reflect the current status of research as well as diagnostic and treatment practices in the field of cancer in the Middle East, where cancer is becoming a growing health problem. Lastly, MEJC would like to become a model for regional journals with an international outlook. Accordingly, manuscripts from authors anywhere in the world will be considered for publication. MEJC will be published on a quarterly basis.
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