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Bioinformatics analysis of microRNA expression between patients with and without latent tuberculosis infections

  • Authors:
    • Yang Lu
    • Xinmin Wang
    • Hongchang Dong
    • Xiaofang Wang
    • Pu Yang
    • Ling Han
    • Yingzi Wang
    • Zhihong Zheng
    • Wanjiang Zhang
    • Le Zhang

  • View Affiliations

  • Published online on: March 20, 2019     https://doi.org/10.3892/etm.2019.7424
  • Pages: 3977-3988

  • Copyright: © Lu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Tuberculosis (TB) is a globally prevalent infectious disease. The mechanisms of latent TB infection (LTBI) remain to be fully elucidated and may provide novel approaches for diagnosis. As therapeutic targets and molecular diagnostic markers, microRNAs (miRs) have been studied and utilized in various diseases. In the present study, the differentially expressed miRs (DEMs) in LTBI were screened and analyzed to determine the underlying mechanisms and identify potential biomarkers, thereby contributing to the diagnosis of LTBI. The GSE25435 and GSE29190 datasets from Gene Expression Omnibus were selected for analysis. The 2 datasets were analyzed individually using the Bioconductor package to screen the DEMs with specific cut‑off criteria [P<0.01 and |log (fold change)|≥1]. Target gene prediction and interaction network construction were performed using Targetscan, the Search Tool for the Retrieval of Interacting Genes and Proteins and Cytoscape individually, and were merged using the latter tool. The hub genes were finally selected based on their degree of connectivity (DC). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed using the KEGG and GENCLIP. A total of 144 DEMs were identified from the 2 datasets. By exploring the overlapping miRs in the two datasets, Homo sapiens (hsa)‑miR‑29a and hsa‑miR‑15b were identified to be decreased, while hsa‑miR‑576‑5p, hsa‑miR‑500 and hsa‑miR‑155 were identified to be upregulated. hsa‑miR‑500a‑3p and hsa‑miR‑29a‑3p, as well as 4 genes, namely cell division cycle (CDC)42, actin α1, skeletal muscle (ACTA1), phosphatase and tensin homolog (PTEN) and fos proto‑oncogene (FOS), were selected as the key factors in this regulatory network. A total of 9 signaling pathways, including phosphoinositide‑3 kinase (PI3K)/AKT and 11 biological processes, were identified to be associated with LTBI. In conclusion, the present analysis identified hsa‑miR‑500a‑3p and hsa‑miR‑29a‑3p, as well as CDC42, ACTA1, PTEN and FOS, as the most promising biomarkers and therapeutic candidates for LTBI. The PI3K/AKT signaling pathway is the key signaling pathway implicated in LTBI, and an in‑depth investigation of the efficiency of PI3K/AKT signaling inhibitors may be used to prevent a chronic state of infection in LTBI.
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May-2019
Volume 17 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Lu Y, Wang X, Dong H, Wang X, Yang P, Han L, Wang Y, Zheng Z, Zhang W, Zhang L, Zhang L, et al: Bioinformatics analysis of microRNA expression between patients with and without latent tuberculosis infections. Exp Ther Med 17: 3977-3988, 2019.
APA
Lu, Y., Wang, X., Dong, H., Wang, X., Yang, P., Han, L. ... Zhang, L. (2019). Bioinformatics analysis of microRNA expression between patients with and without latent tuberculosis infections. Experimental and Therapeutic Medicine, 17, 3977-3988. https://doi.org/10.3892/etm.2019.7424
MLA
Lu, Y., Wang, X., Dong, H., Wang, X., Yang, P., Han, L., Wang, Y., Zheng, Z., Zhang, W., Zhang, L."Bioinformatics analysis of microRNA expression between patients with and without latent tuberculosis infections". Experimental and Therapeutic Medicine 17.5 (2019): 3977-3988.
Chicago
Lu, Y., Wang, X., Dong, H., Wang, X., Yang, P., Han, L., Wang, Y., Zheng, Z., Zhang, W., Zhang, L."Bioinformatics analysis of microRNA expression between patients with and without latent tuberculosis infections". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3977-3988. https://doi.org/10.3892/etm.2019.7424