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miR-144-3p表达上调通过靶向BCL6减弱胶质瘤细胞的活力和侵袭能力。

Upregulation of miR-144-3p expression attenuates glioma cell viability and invasion by targeting BCL6.

作者信息

Zhou Jingru, Liu Ruen

机构信息

Department of Neurosurgery, Nanchang University People's Hospital, Nanchang, Jianxi 330006, P.R. China.

Department of Neurosurgery, Peking University People's Hospital, Beijing 100044, P.R. China.

出版信息

Exp Ther Med. 2021 Oct;22(4):1157. doi: 10.3892/etm.2021.10591. Epub 2021 Aug 10.

DOI:10.3892/etm.2021.10591
PMID:34504602
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8393981/
Abstract

Glioma remains to be an aggressive type of cancer with poor prognosis irrespective of the type of standard treatment applied. Therefore, identification of accurate early diagnostic methods and therapeutic strategies for glioma is imperative for the treatment of this disease. The expression of a number of miRNAs in glioma have been reported to be associated with the regulation of tumorigenic progression, cancer cell proliferation, metastasis, invasion, angiogenesis and drug resistance. The aim of the present study was to assess the function of the microRNA (miR/miRNA)-144-3p/BCL6 axis in glioma. Reverse transcription-quantitative PCR was used to measure miR-144-3p and BCL6 expression. Western blotting was used for measuring BCL6 expression. Luciferase reporter assay was used to assess the association between miR-144-3p and BCL6 and a tumor xenograft model was established for assess tumor growth. The data demonstrated that miR-144-3p was decreased whereas BCL6 expression was increased in glioma tissues compared with those in healthy human brain tissues, where miR-144-3p suppressed BCL6 expression by targeting the 3'-UTR sequence of BCL6. miR-144-3p overexpression alleviated proliferation and invasion in U251 cells whereas transfection with the BCL6-overexpressing plasmid rescued the suppressive effects of miR-144-3p upregulation on the proliferation and invasion of U251 cells. In addition, miR-144-3p overexpression and BCL6 downregulation inhibited tumor progression in a mouse tumor xenograft model. The present findings suggest that miR-144-3p and BCL6 may serve to be indicator of proliferation and invasion for patients with glioma. Furthermore, BCL6 may serve an important role in the miR-144-3p-mediated regulation of proliferation and invasion of glioma cells, where the miR-144-3p/BCL6 axis can be used to target patients with glioma therapeutically.

摘要

无论采用何种标准治疗方式,胶质瘤仍然是一种侵袭性癌症,预后较差。因此,确定准确的早期诊断方法和胶质瘤治疗策略对于治疗这种疾病至关重要。据报道,胶质瘤中多种微小RNA(miR/miRNA)的表达与肿瘤发生进展、癌细胞增殖、转移、侵袭、血管生成和耐药性的调节有关。本研究的目的是评估微小RNA(miR/miRNA)-144-3p/BCL6轴在胶质瘤中的作用。采用逆转录定量PCR检测miR-144-3p和BCL6的表达。采用蛋白质印迹法检测BCL6的表达。采用荧光素酶报告基因检测法评估miR-144-3p与BCL6之间的关联,并建立肿瘤异种移植模型评估肿瘤生长。数据表明,与健康人脑组织相比,胶质瘤组织中miR-144-3p表达降低,而BCL6表达升高,其中miR-144-3p通过靶向BCL6的3'-UTR序列抑制BCL6表达。miR-144-3p过表达减轻了U251细胞的增殖和侵袭,而转染BCL6过表达质粒则挽救了miR-144-3p上调对U251细胞增殖和侵袭的抑制作用。此外,miR-144-3p过表达和BCL6下调抑制了小鼠肿瘤异种移植模型中的肿瘤进展。本研究结果表明,miR-144-3p和BCL6可能是胶质瘤患者增殖和侵袭的指标。此外,BCL6可能在miR-144-3p介导的胶质瘤细胞增殖和侵袭调节中起重要作用,其中miR-144-3p/BCL6轴可用于胶质瘤患者的治疗靶点。

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MicroRNA-144-3p Inhibits Tumorigenesis of Oral Squamous Cell Carcinoma by downregulating ERO1L.微小RNA-144-3p通过下调ERO1L抑制口腔鳞状细胞癌的肿瘤发生。
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MicroRNA-144-3p suppressed TGF-β1-induced lung cancer cell invasion and adhesion by regulating the Src-Akt-Erk pathway.微小RNA-144-3p通过调节Src-Akt-Erk信号通路抑制转化生长因子-β1诱导的肺癌细胞侵袭和黏附。
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miR-144-3p facilitates nasopharyngeal carcinoma via crosstalk with PTEN.miR-144-3p 通过与 PTEN 的相互作用促进鼻咽癌的发生。
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