Bioinformatics facilitating the use of microarrays to delineate potential miRNA biomarkers in aristolochic acid nephropathy

Lv, Yana; Que, Yumei; Su, Qiao; Li, Qiang; Chen, Xi; Lü, Haitao

doi:10.18632/oncotarget.10586

Cited by 3 publications

(2 citation statements)

References 67 publications

(62 reference statements)

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“…In recent years, more than 30 microRNAs differentially expressed in patients exposed to AAs have been explored, which might improve the understanding of the pathogenesis of AA-related renal disease and cancer. It has been speculated that FGFR3, Akt, mucin type O-glycan biosynthesis, ECM receptor interaction pathways, and other biological mechanisms might be involved in the occurrences of AAN, BEN, and/or AA-induced UTUC (Tao et al, 2015; Lv et al, 2016; Popovska-Jankovic et al, 2016). Meanwhile, 15% of the 417 detectable miRNAs have been found to be altered by AAs in rats (Li et al, 2015).…”

Section: Toxicological Properties Of Aristolochic Acidsmentioning

confidence: 99%

Systematic Overview of Aristolochic Acids: Nephrotoxicity, Carcinogenicity, and Underlying Mechanisms

et al. 2019

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Aristolochic acids (AAs) are a group of toxins commonly present in the plants of genus Aristolochia and Asarum , which are spread all over the world. Since the 1990s, AA-induced nephropathy (AAN) and upper tract urothelial carcinoma (UTUC) have been reported in many countries. The underlying mechanisms of AAN and AA-induced UTUC have been extensively investigated. AA-derived DNA adducts are recognized as specific biomarkers of AA exposure, and a mutational signature predominantly characterized by A→T transversions has been detected in AA-induced UTUC tumor tissues. In addition, various enzymes and organic anion transporters are involved in AA-induced adverse reactions. The progressive lesions and mutational events initiated by AAs are irreversible, and no effective therapeutic regimen for AAN and AA-induced UTUC has been established until now. Because of several warnings on the toxic effects of AAs by the US Food and Drug Administration and the regulatory authorities of some other countries, the sale and use of AA-containing products have been banned or restricted in most countries. However, AA-related adverse events still occur, especially in the Asian and Balkan regions. Therefore, the use of AA-containing herbal remedies and the consumption of food contaminated by AAs still carry high risk. More strict precautions should be taken to protect the public from AA exposure.

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Section: Toxicological Properties Of Aristolochic Acidsmentioning

confidence: 99%

Systematic Overview of Aristolochic Acids: Nephrotoxicity, Carcinogenicity, and Underlying Mechanisms

et al. 2019

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“…In a disease network, a systems biology approach can be adopted as a means to reveal complex molecular interactions, rather than single molecular components ( 6 ). The ‘omics’ analyses, which represent major cornerstones of systems biology research, are considered to be unbiased methods for the identification of biomarkers and to elucidate the pathological mechanisms of chronic kidney disease ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses

Liu

Shang

et al. 2018

Mol Med Report

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Hypertensive nephrosclerosis (HNS) is a major risk factor for end-stage renal disease. However, the underlying pathogenesis of HNS remains to be fully determined. The gene expression profile of GSE20602, which consists of 14 glomeruli samples from patients with HNS and 4 normal glomeruli control samples, was obtained from the Gene Expression Omnibus database. Gene ontology (GO) and pathway enrichment analyses were performed in order to investigate the functions and pathways of differentially expressed genes (DEGs). Pathway relation and co-expression networks were constructed in order to identify key genes and signaling pathways involved in HNS. In total, 483 DEGs were identified to be associated with HNS, including 302 upregulated genes and 181 downregulated genes. Furthermore, GO analysis revealed that DEGs were significantly enriched in the small molecule metabolic process. In addition, pathway analysis also revealed that DEGs were predominantly involved in metabolic pathways. The tricarboxylic acid (TCA) cycle was identified as the hub pathway in the pathway relation network, whereas the sorbitol dehydrogenase (SORD) and cubulin (CUBN) genes were revealed to be the hub genes in the co-expression network. The present study revealed that the SORD, CUBN and albumin genes as well as the TCA cycle and metabolic pathways are involved in the pathogenesis of HNS. The results of the present study may contribute to the determination of the molecular mechanisms underlying HNS, and provide insight into the exploration of novel targets for the diagnosis and treatment of HNS.

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TNF-α-induced miR-450a mediates TMEM182 expression to promote oral squamous cell carcinoma motility

et al. 2019

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Distant metastasis leads oral cancer patients into a poor survival rate and a high recurrence stage. During tumor progression, dysregulated microRNAs (miRNAs) have been reported to involve tumor initiation and modulate oral cancer malignancy. MiR-450a was significantly upregulated in oral squamous cell carcinoma (OSCC) patients without functional reports. This study was attempted to uncover the molecular mechanism of novel miR-450a in OSCC. Mir-450a expression was examined by quantitative RT-PCR, both in OSCC cell lines and patients. Specific target of miR-450a was determined by software prediction, luciferase reporter assay, and correlation with target protein expression. The functions of miR-450a and TMEM182 were accessed by adhesion and transwell invasion analyses. Determination of the expression and cellular localization of TMEM182 was examined by RT-PCR and by immunofluorescence staining. The signaling pathways involved in regulation of miR-450a were investigated using the kinase inhibitors. Overexpression of miR-450a in OSCC cells impaired cell adhesion ability and induced invasiveness, which demonstrated the functional role of miR-450a as an onco-miRNA. Interestingly, tumor necrosis factor alpha (TNF-α)-mediated expression of TMEM182 was regulated by miR-450a induction. MiR-450a-reduced cellular adhesion was abolished by TMEM182 restoration. Furthermore, the oncogenic activity of TNF-α/miR-450a/TMEM182 axis was primarily through activating extracellular signal–regulated kinase 1/2 (ERK1/2) signaling pathway. ERK1/2 inhibitor prevented the TNF-α-induced miR-450a expression and enhanced adhesion ability. Our data suggested that TNF-α-induced ERK1/2-dependent miR-450a against TMEM182 expression exerted a great influence on increasing OSCC motility. Overall, our results provide novel molecular insights into how TNF-α contributes to oral carcinogenesis through miR-450a that targets TMEM182.

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Bioinformatics facilitating the use of microarrays to delineate potential miRNA biomarkers in aristolochic acid nephropathy

Cited by 3 publications

References 67 publications

Systematic Overview of Aristolochic Acids: Nephrotoxicity, Carcinogenicity, and Underlying Mechanisms

Systematic Overview of Aristolochic Acids: Nephrotoxicity, Carcinogenicity, and Underlying Mechanisms

Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses

TNF-α-induced miR-450a mediates TMEM182 expression to promote oral squamous cell carcinoma motility

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