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Whole-transcriptome sequencing analysis to identify key non-coding RNAs in the pathogenesis of pulmonary tuberculosis

Aug 2026 · Public Health Action · Vol 16, pp. 281 - 287 · 0 citations · 20 references
Medicine

TL;DR

It is suggested that differentially expressed ncRNAs may play a role in the pathogenesis of TB and the circRNA and the hub mRNA are potential candidates for further exploration as biomarkers for TB infection.

Abstract

Background

Non-coding RNAs (ncRNAs) have been shown to play essential roles in various human diseases, including pulmonary tuberculosis (TB). This study aims to investigate differentially expressed ncRNAs, explore their potential biological functions, and determine whether they can serve as biomarkers and therapeutic targets in TB.

Methods

Whole-transcriptome RNA sequencing was performed on blood samples from TB patients and healthy controls (n = 3 per group). Differentially expressed mRNAs, long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs) were identified, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. A competing endogenous RNA (ceRNA) network was constructed, and hub genes were identified via protein–protein interaction network analysis using Cytoscape.

Results

A total of 507 differentially expressed mRNAs, 107 differentially expressed lncRNAs, 253 differentially expressed circRNAs, and 38 differentially expressed miRNAs were identified. Functional enrichment revealed involvement in pathways related to cellular processes, mTOR signalling, and endocytosis. A circRNA–miRNA–mRNA ceRNA network was constructed, and hub mRNAs including RACK1, EIF3G, and RPS15 were identified.

Conclusion

It is suggested that differentially expressed ncRNAs may play a role in the pathogenesis of TB. The circRNA (hsa_circ_0003340) and the hub mRNA (RACK1) are potential candidates for further exploration as biomarkers for TB infection. Moreover, the ceRNA network constructed in this study may provide new insights into the regulatory mechanisms of TB.

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