FOXC2介导的ADAM12沉默通过抑制JAK1/STAT3/VEGFA通路抑制脑膜瘤进展

IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochemical Genetics Pub Date : 2024-07-27 DOI:10.1007/s10528-024-10893-4
Huaming Zhang, Bing Yang
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引用次数: 0

摘要

脑膜瘤是一种常见的颅内肿瘤,恶性程度高,复发率高。解体蛋白和金属蛋白酶 12(ADAM12)是一种常见的癌基因,在脑膜瘤中有不同程度的表达。然而,它在脑膜瘤发病过程中的作用和机制仍不明确。研究人员利用 GEO(GSE77259 和 GSE43290)数据集和基于 GSE16581 的加权基因共表达网络分析(WGCNA)分析了脑膜瘤中的差异表达基因。ADAM12的表达通过qRT-PCR和Western印迹检测。通过 JASPER 工具预测了 ADAM12 与 FOXC2 的相关性,并通过荧光素酶报告分析确定了两者的相关性。使用 CCK-8、EdU 和 transwell 试验研究了细胞的增殖、迁移和侵袭。IL-6激活了JAK1/STAT3/VEGFA信号传导,并通过Western印迹进行了分析。通过WGCNA和GEO分析筛选了脑膜瘤中差异表达的ADAM12。沉默ADAM12可抑制脑膜瘤细胞增殖,减少迁移和侵袭。根据 GSE77259 和 GSE43290 数据集,转录因子 FOXC2 在脑膜瘤中表达增强,并正向诱导 ADAM12 的转录。ADAM12沉默导致JAK1/STAT3/VEGFA信号失活,并通过IL-6被激活。FOXC2的上调促进了细胞的增殖、迁移和侵袭,而沉默ADAM12则逆转了这些效应。通过沉默FOXC2介导的ADAM12敲除可以抑制JAK1/STAT3/VEGFA通路,从而抑制脑膜瘤细胞的增殖、迁移和侵袭。
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ADAM12 Silencing Mediated by FOXC2 Represses Meningioma Progression Through Inactivating the JAK1/STAT3/VEGFA Pathway

Meningioma is a prevalently intracranial tumor, and the malignant type is aggressive with high recurrence. A Disintegrin and Metalloprotease 12 (ADAM12) is a common oncogene and differentially expressed in meningioma. However, its roles and mechanisms in meningioma development remain obscure. The differentially expressed genes in meningioma were analyzed by GEO (GSE77259 and GSE43290) datasets and weighted gene co-expression network analysis (WGCNA) based on GSE16581. ADAM12 expression was measured via qRT-PCR and western blot. The correlation between ADAM12 and FOXC2 was predicted through JASPER tool and identified via luciferase reporter analysis. Cell proliferation, migration and invasion were investigated using CCK-8, EdU, transwell assays. The JAK1/STAT3/VEGFA signaling was activated by IL-6, and analyzed via western blot. The differentially expressed ADAM12 in meningioma was screened by WGCNA and GEO analyses. ADAM12 silencing repressed meningioma cell proliferation, and decreased migration and invasion. The transcription factor FOXC2 expression was enhanced in meningioma based on GSE77259 and GSE43290 datasets, and positively induced ADAM12 transcription. The JAK1/STAT3/VEGFA signaling was inactivated due to ADAM12 silencing and activated via IL-6. Upregulation of FOXC2 promoted cell proliferation, migration and invasion, and these effects were reversed by silencing ADAM12. ADAM12 knockdown mediated via FOXC2 silencing restrained proliferation, migration and invasion of meningioma cells through inactivating the JAK1/STAT3/VEGFA pathway.

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来源期刊
Biochemical Genetics
Biochemical Genetics 生物-生化与分子生物学
CiteScore
3.90
自引率
0.00%
发文量
133
审稿时长
4.8 months
期刊介绍: Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses. Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication. Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses. Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods. Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.
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