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采用联合 DNA、mRNA 和蛋白质分析鉴定黏液样脂肪肉瘤中调节细胞增殖和 FUS-DDIT3 表达的抑制剂。

Identification of inhibitors regulating cell proliferation and FUS-DDIT3 expression in myxoid liposarcoma using combined DNA, mRNA, and protein analyses.

机构信息

Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at University of Gothenburg, Medicinaregatan 1F, 413 90, Gothenburg, Sweden.

Laboratory of gene expression, Institute of Biotechnology AS CR, BIOCEV, Prumyslova 595, 252 50, Vestec by Prague, Czech Republic.

出版信息

Lab Invest. 2018 Jul;98(7):957-967. doi: 10.1038/s41374-018-0046-3. Epub 2018 Mar 27.

DOI:10.1038/s41374-018-0046-3
PMID:29588491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6070472/
Abstract

FUS-DDIT3 belongs to the FET (FUS, EWSR1, and TAF15) family of fusion oncogenes, which collectively are considered to be key players in tumor development. Even though over 90% of all myxoid liposarcomas (MLS) have a FUS-DDIT3 gene fusion, there is limited understanding of the signaling pathways that regulate its expression. In order to study cell proliferation and FUS-DDIT3 regulation at mRNA and protein levels, we first developed a direct cell lysis approach that allows DNA, mRNA, and protein to be analyzed in the same sample using quantitative PCR, reverse transcription quantitative qPCR and proximity ligation assay, respectively. We screened 70 well-characterized kinase inhibitors and determined their effects on cell proliferation and expression of FUS-DDIT3 and FUS at both mRNA and protein levels in the MLS 402-91 cell line, where twelve selected inhibitors were evaluated further in two additional MLS cell lines. Both FUS-DDIT3 and FUS mRNA expression correlated with cell proliferation and both transcripts were co-regulated in most conditions, indicating that the common 5' FUS promotor is important in transcriptional regulation. In contrast, FUS-DDIT3 and FUS protein levels displayed more cell line dependent expression. Furthermore, most JAK inhibitors caused FUS-DDIT3 downregulation at both mRNA and protein levels. In conclusion, defining factors that regulate FUS-DDIT3 expression opens new means to understand MLS development at the molecular level.

摘要

FUS-DDIT3 属于 FET(FUS、EWSR1 和 TAF15)融合癌基因家族,它们共同被认为是肿瘤发展的关键因素。尽管超过 90%的黏液样脂肪肉瘤(MLS)都有 FUS-DDIT3 基因融合,但对于调节其表达的信号通路的了解有限。为了研究细胞增殖和 FUS-DDIT3 在 mRNA 和蛋白质水平上的调控,我们首先开发了一种直接细胞裂解方法,该方法允许使用定量 PCR、逆转录定量 qPCR 和接近连接测定法分别在同一样本中分析 DNA、mRNA 和蛋白质。我们筛选了 70 种经过充分验证的激酶抑制剂,并确定了它们对 MLS 402-91 细胞系中细胞增殖以及 FUS-DDIT3 和 FUS 在 mRNA 和蛋白质水平上表达的影响,然后在另外两个 MLS 细胞系中进一步评估了 12 种选定的抑制剂。FUS-DDIT3 和 FUS mRNA 表达均与细胞增殖相关,并且在大多数情况下,这两个转录物均受到共同调控,这表明共同的 5' FUS 启动子在转录调控中很重要。相比之下,FUS-DDIT3 和 FUS 蛋白质水平的表达更依赖于细胞系。此外,大多数 JAK 抑制剂会导致 FUS-DDIT3 在 mRNA 和蛋白质水平上的下调。总之,确定调节 FUS-DDIT3 表达的因素为在分子水平上理解 MLS 的发展开辟了新的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/adcdc53f4cfe/41374_2018_46_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/0049994e13ef/41374_2018_46_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/9785f4b30579/41374_2018_46_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/889fd1c9e39d/41374_2018_46_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/adcdc53f4cfe/41374_2018_46_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/0049994e13ef/41374_2018_46_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/9785f4b30579/41374_2018_46_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/889fd1c9e39d/41374_2018_46_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e56/6070472/adcdc53f4cfe/41374_2018_46_Fig4_HTML.jpg

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