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Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 70-74

Upregulated bovine tuberculosis microRNAs Trigger oncogenic pathways: An In silico perception

1 Department of Animal Production and Fisheries, Laboratory of Animal Physiology and Health, Institute of Agricultural Research for Development, Bambui, Cameroon
2 Department of Computational Biology and Bioinformatics, University of Kerala, Thiruvananthapuram, Kerala, India
3 Division of Immunology and South Africa Medical Research Council, Immunology of Infectious Disease, Faculty of Health Sciences, University of Cape Town, Institute of Infectious Diseases and Molecular Medicine, South Africa; Department of Biochemistry, University of Douala, Cameroon
4 System Biology Laboratory, Chantal Biya International Reference Center, Yaounde; Department of Biology, Higher Teachers' Training College, University of Yaounde I, Cameroon

Correspondence Address:
Elvis Ndukong Ndzi
Laboratory of Animal Physiology and Health, Institute of Agricultural Research for Development, P. O. Box 51, Irad Bambui
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijmy.ijmy_9_19

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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.

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