Background: Acute kidney injury (AKI) refers to a sudden loss of renal function. This study was performed to identify the key RNAs acting in the mechanism of sepsis-induced AKI.Methods: Microarray dataset GSE94717 (including six sepsis-induced AKI samples and three control samples) was downloaded from Gene Expression Omnibus database. Differentially expressed miRNAs (DE-miRNAs) were identified. The miRNA targets were predicted and enrichment analysis was performed. Protein-protein interaction (PPI) and competing endogenous RNA (ceRNA) regulatory networks were constructed. Mouse podocytes were treated with lipopolysaccharide (LPS), following by cell viability and PCR analysis. Cellular apoptosis and the ceRNA network were validated.Results: Thirty-one common DE-miRNAs (two up-regulated and 29 down-regulated) by AKI versus control and male AKI versus control were identified. We found the targets of miR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway, and those of miR-29b-3p and miR-16-5p were enriched in PI3K-Akt signaling pathway. RNAs including miR-15b-5p, miR-15a-5p, miR-107, XIST, miR-16-5p, and cullin 3 gene (CUL3) were included in the ceRNA regulatory network. The downregulation of miR-15a-5p and miR-15b-5p and the upregulation of lncRNA XIST and CUL3 gene were validated using qPCR. The miR-15a-5p-XIST-CUL3 regulatory axis was identified and was validated. We confirmed that LPS inhibited the growth of mouse podocytes and seven of the ten miRNAs, but upregulated XIST and CUL3. Transfection analysis showed XIST siRNA enhanced LPS-induced MPC5 cell apoptosis and miR-15a-5p inhibitor reserved it, so did as CUL3 overexpression for miR-15a-5p mimics.Conclusion: The miR-15a-5p-XIST-CUL3 regulatory axis was related to the pathogenesis of sepsis-induced AKI.HighlightsTotally, 31 miRNAs were dysregulated between disease and control groups.MiR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway.MiR-16-5p and miR-29b-3p were implicated in PI3K-Akt signaling pathway.The miR-15a-5p-XIST-CUL3 axis was critical for sepsis-induced AKI.

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Nasopharyngeal carcinoma (NPC) is one of the malignant epithelial tumors with a high metastasis rate. This study aimed to screen potential novel biomarkers involved in NPC metastasis. Microarray data of locoregionally advanced NPC (LA-NPC; GSE103611) were obtained from the database of Gene Expression Omnibus. The differentially expressed genes (DEGs) between LA-NPC tissues with and without distant metastasis after radical treatment were screened. Functional analysis was performed and the protein–protein interaction and submodule were analyzed. The univariate Cox regression analysis was performed to identify prognostic genes in NPC in the validation microarray dataset GSE102349. The drug–gene interactions and key genes were identified. Totally, 107 DEGs were identified. The upregulated DEGs and the key nodes in the protein–protein interaction network were associated with pathways or biological processes related to the cell cycle. Four genes including CD44, B2M, PTPN11, and TRIM74 were associated with disease-free survival in NPC. The drug–gene interaction analysis revealed that upregulated genes CXCL10, CD44, B2M, XRCC5, and RPL11 might be potential druggable genes for patients with LA-NPC metastasis by regulating cell cycle, autophagy, and drug resistance. Upregulated CXCL10, CD44, B2M, XRCC5, and RPL11 might play important roles in LA-NPC metastasis by regulating cell cycle-related pathways.