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成纤维细胞生长因子轴与 miR-16 家族之间的联系揭示了间皮瘤中潜在的新治疗组合。

A link between the fibroblast growth factor axis and the miR-16 family reveals potential new treatment combinations in mesothelioma.

机构信息

Asbestos Diseases Research Institute, Sydney, Australia.

Department of Medicine I, Institute of Cancer Research, Medical University of Vienna, Austria.

出版信息

Mol Oncol. 2018 Jan;12(1):58-73. doi: 10.1002/1878-0261.12150. Epub 2017 Nov 18.

DOI:10.1002/1878-0261.12150
PMID:29094504
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5748487/
Abstract

Malignant pleural mesothelioma (MPM) is an aggressive malignancy with very limited therapeutic options. Fibroblast growth factor (FGF) signals play important roles in mesothelioma cell growth. Several FGFs and FGF receptors (FGFRs) are predicted targets of the miR-15/16 family, which is downregulated in MPM. The aim of this study was to explore the link between the miR-15/16 family and the FGF axis in MPM. Expression analyses via RT-qPCR showed downregulation of the FGF axis after transfection with miR-15/16 mimics. Direct interaction was confirmed by luciferase reporter assays. Restoration of miR-15/16 led to dose-dependent growth inhibition in MPM cell lines, which significantly correlated with their sensitivity to FGFR inhibition. Treatment with recombinant FGF2 prevented growth inhibition and further reduced the levels of FGF/R-targeting microRNAs, indicating a vicious cycle between miR-15/16 down- and FGF/FGFR signaling upregulation. Combined inhibition of two independent miR-15/16 targets, the FGF axis and Bcl-2, resulted in additive or synergistic activity. Our data indicate that post-transcriptional repression of FGF-mediated signals contributes to the tumor suppressor function of the microRNA-15/16 family. Inhibiting hyperactivated FGF signals and Bcl-2 might serve as a novel therapeutic combination strategy in MPM.

摘要

恶性胸膜间皮瘤(MPM)是一种侵袭性恶性肿瘤,治疗选择非常有限。成纤维细胞生长因子(FGF)信号在间皮瘤细胞生长中发挥重要作用。几种 FGF 和 FGF 受体(FGFRs)被预测为 miR-15/16 家族的靶标,miR-15/16 家族在 MPM 中下调。本研究旨在探讨 miR-15/16 家族与 MPM 中 FGF 轴之间的联系。通过 RT-qPCR 的表达分析显示,转染 miR-15/16 模拟物后 FGF 轴下调。荧光素酶报告基因检测证实了直接相互作用。miR-15/16 的恢复导致 MPM 细胞系的剂量依赖性生长抑制,这与它们对 FGFR 抑制的敏感性显著相关。用重组 FGF2 处理可防止生长抑制,并进一步降低 FGF/R 靶向 microRNAs 的水平,表明 miR-15/16 下调和 FGF/FGFR 信号上调之间存在恶性循环。两种独立的 miR-15/16 靶标,即 FGF 轴和 Bcl-2 的联合抑制导致相加或协同作用。我们的数据表明,FGF 介导的信号的转录后抑制有助于 microRNA-15/16 家族的肿瘤抑制功能。抑制过活化的 FGF 信号和 Bcl-2 可能是 MPM 的一种新的治疗联合策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/175edf6a897a/MOL2-12-58-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/6669311e4deb/MOL2-12-58-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/4b59a3e99fba/MOL2-12-58-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/2fef561d270e/MOL2-12-58-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/1d365d1413fd/MOL2-12-58-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/cb880210e28a/MOL2-12-58-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/175edf6a897a/MOL2-12-58-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/6669311e4deb/MOL2-12-58-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/4b59a3e99fba/MOL2-12-58-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/2fef561d270e/MOL2-12-58-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/1d365d1413fd/MOL2-12-58-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/cb880210e28a/MOL2-12-58-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6bc/5748487/175edf6a897a/MOL2-12-58-g006.jpg

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