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上调的牛结核病微小RNA触发致癌途径:一种认识。

Upregulated bovine tuberculosis microRNAs Trigger oncogenic pathways: An perception.

作者信息

Ndzi Elvis Ndukong, Indu Viswanath Ambily Nath, Adzemye Nsadzetsen Gilbert, Tamgue Ousman, Nsongka Munji Victorine, Nair Achuthsankar S, Nkenfou Céline Nguefeu

机构信息

Department of Animal Production and Fisheries, Laboratory of Animal Physiology and Health, Institute of Agricultural Research for Development, Bambui, Cameroon.

Department of Computational Biology and Bioinformatics, University of Kerala, Thiruvananthapuram, Kerala, India.

出版信息

Int J Mycobacteriol. 2019 Jan-Mar;8(1):70-74. doi: 10.4103/ijmy.ijmy_9_19.

Abstract

BACKGROUND/OBJECTIVE: Although microRNA (miRNA)-directed regulation of bovine tuberculosis (bTB) has already been reported, very little is known about the incited pathways and genes. We profiled bTB-upregulated miRNAs through an in silico methodology.

METHODS

The data of upregulated miRNAs in bTB versus healthy controls were collected and clustered into three groups by their tissue specificity as follows: G1 (mammary gland-specific): bta-miR-146a; G2 (peripheral blood mononuclear cell-specific): bta-miR-155; and G3 (alveolar macrophage-specific): bta-miR-146a, bta-miR-155, bta-miR-142-5p, bta-miR-423-3p, bta-miR-21-5p, bta-miR-27a-3p, bta-miR-99b, bta-miR-147, bta-miR-223, and bta-let-7i. The miRNA-mRNA interaction network was defined by TargetScan. The gene ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways of these transcripts were examined.

RESULTS

The results illustrate the induction of pathways in cancer, highly enriched, and unanimous to all three gene sets (G1, G2, and G3). Mitogen-activated protein kinase and PI3K-Akt signaling were specific to G2 and G3 with fibroblast growth factors formed the key factors.

CONCLUSION

The inferred cancer cascades denote a probable modulation of innate immune response in an infectious state. These baseline pictures could lay the ground for further substantive studies.

摘要

背景/目的:尽管已有关于微小RNA(miRNA)对牛结核病(bTB)的调控报道,但对所引发的信号通路和基因却知之甚少。我们通过计算机模拟方法分析了bTB上调的miRNA。

方法

收集bTB与健康对照中上调miRNA的数据,并根据其组织特异性分为三组:G1组(乳腺特异性):bta-miR-146a;G2组(外周血单核细胞特异性):bta-miR-155;G3组(肺泡巨噬细胞特异性):bta-miR-146a、bta-miR-155、bta-miR-142-5p、bta-miR-423-3p、bta-miR-21-5p、bta-miR-27a-3p、bta-miR-99b、bta-miR-147、bta-miR-223和bta-let-7i。通过TargetScan确定miRNA-mRNA相互作用网络。研究这些转录本的基因本体术语和京都基因与基因组百科全书通路。

结果

结果表明癌症相关信号通路被诱导,在所有三个基因集(G1、G2和G3)中高度富集且一致。丝裂原活化蛋白激酶和PI3K-Akt信号通路对G2和G3组具有特异性,成纤维细胞生长因子是关键因素。

结论

推测的癌症级联反应表明感染状态下固有免疫反应可能受到调节。这些基础情况可为进一步的实质性研究奠定基础。

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