MicroRNAs-mRNAs Expression Profile and Their Potential Role in Malignant Transformation of Human Bronchial Epithelial Cells Induced by Cadmium

Luo, Qun; Zheng, Chengbin; Shen, Huanyu; Zhang, Zhiheng; Lei, Yixiong

doi:10.1155/2015/902025

Cited by 27 publications

(14 citation statements)

References 43 publications

(38 reference statements)

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“…The analysis results showed that the 954 genes were enriched in tumor-associated pathways, such as non-small cell lung cancer, small cell lung cancer, thyroid cancer, pancreatic cancer, chronic myeloid leukemia, and so forth, suggesting that chronic arsenite exposure confers characteristics of tumor cells to HBE cells via regulating various cancer pathways. The results were supported by a previous report in which the cancer-associated pathways were also activated in the malignant transformed cells induced by cadmium [ 37 ].…”

Section: Discussionsupporting

confidence: 90%

Alterations of miRNAs and Their Potential Roles in Arsenite-Induced Transformation of Human Bronchial Epithelial Cells

Sun

et al. 2017

Genes

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The alterations of micro RNAs (miRNAs) and their potential roles in arsenite-induced tumorigenesis are still poorly understood. In this study, miRNA Array was used to detect the expression level of miRNAs in human bronchial epithelial (HBE) cells that were transformed by 2.5 μM arsenite for 13 weeks. These cells exhibited a neoplastic phenotype manifested by increased levels of cellular proliferation and migration and clone formation. Subsequently, 191 dysregulated miRNAs were identified to be associated with arsenite-induced transformation by miRNA Array. Among them, six miRNAs were validated by their expression levels with quantitative real-time polymerase chain reaction (qPCR), and 17 miRNAs were further explored via their target genes as well as regulatory network. Three databases, TargetMiner, miRDB, and TarBase, were used to predict the target genes of the 17 miRNAs, and a total of 954 common genes were sorted. Results of Gene Ontology (GO) analyses showed that the 954 genes were involved in diverse terms of GO categories, such as positive regulation of macroautophagy, epithelial cell maturation, and synaptic vesicle clustering. Moreover, results of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses demonstrated that most of these target genes were enriched in various cancer-related pathways, including non-small cell lung cancer, Wnt signaling pathway, cell cycle, and p53 signaling pathway. The miRNA-gene regulatory network, which was constructed by cytoscape software with miRNAs and their target genes, showed that miR-15b-5p, miR-106b-5p, and miR-320d were the core hubs. Collectively, our results provide new insights into miRNA-mediated mechanisms underlying arsenite-induced transformation, although more experimental verification is still needed to prove these predictions.

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Section: Discussionsupporting

confidence: 90%

Alterations of miRNAs and Their Potential Roles in Arsenite-Induced Transformation of Human Bronchial Epithelial Cells

Sun

et al. 2017

Genes

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“…The normal function of p53 in regulating apoptosis and cellular function and repair is necessary to maintain normal cell function and prevent cancer development. In bronchial epithelial cells, Cd exposure via cigarette smoking can modify multiple miRNA by both up-and downregulation [70].…”

Section: Cadmium-associated Changes In Mirna Expressionmentioning

confidence: 99%

Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development

Wallace

Taalab

Heinze

et al. 2020

Cells

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Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)-short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain-a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs).

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“…Although the underlying mechanisms associated with Cd exposure have not been addressed in COPD, recent studies have suggested that Cd is closely associated with the severity and progression of COPD (8)(9)(10). Furthermore, exposure to Cd leads to epigenetic modulations, including aberrant methylation of DNA repair genes, histone modification, or microRNAs (miRNAs) (11)(12)(13).…”

Section: Original Articlementioning

confidence: 99%

Role of miRNA-181a-2-3p in cadmium-induced inflammatory responses of human bronchial epithelial cells

Kim¹,

Kim²,

Heo³

et al. 2019

J. Thorac. Dis

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Background: Inflammation is an important priming event in the pathogenesis of pulmonary diseases, including chronic obstructive pulmonary disease (COPD). Increasing evidence indicates that microRNAs (miRNAs) contribute to the pathogenesis of COPD by regulating inflammatory response. Therefore, it is necessary to investigate novel molecular targets in COPD without any validation in COPD samples in airway inflammation. The aim of our study is to reveal novel miRNAs that can influence molecular targets for COPD and to examine the underlying mechanism in airway inflammation. Methods: We identified the downregulation of miR-181a-2-3p in the serum of COPD patients and further investigated the role of miR-181a-2-3p in cadmium (Cd)-induced inflammation of a human bronchial epithelial cell line (BEAS-2B) and normal human bronchial epithelial (NHBE) cells. Results: Our results showed that expression of miR-181a-2-3p was significantly decreased in Cd-treated cells and silencing of miR-181a-2-3p enhanced Cd-induced inflammatory responses and inflammasome activation. This negative regulatory effect of miR-181a-2-3p on inflammation is partly mediated by the calcium signaling pathway. Furthermore, global gene expression profiling revealed that Toll-like receptor 4 or sequestosome 1 genes were identified as potential targets of miR-181a-2-3p, which were significantly upregulated by knockdown of miR-181a-2-3p in Cd-treated cells. Conclusions: Our results strongly suggest that miR-181a-2-3p has a critical role in Cd-induced inflammation of airway by regulating its potential target genes, which could be molecular targets for COPD.

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MicroRNAs-mRNAs Expression Profile and Their Potential Role in Malignant Transformation of Human Bronchial Epithelial Cells Induced by Cadmium

Cited by 27 publications

References 43 publications

Alterations of miRNAs and Their Potential Roles in Arsenite-Induced Transformation of Human Bronchial Epithelial Cells

Alterations of miRNAs and Their Potential Roles in Arsenite-Induced Transformation of Human Bronchial Epithelial Cells

Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development

Role of miRNA-181a-2-3p in cadmium-induced inflammatory responses of human bronchial epithelial cells

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