Analysis of the miRNA–mRNA networks in malignant transformation BEAS-2B cells induced by alpha-particles

Nie, Jing; Chen, Zhi-Hai; Shao, Chunlin; Pei, Weiwei; Zhang, Jie; Zhang, Shuyu; Jiao, Yang; Tong, Jian

doi:10.1080/15287394.2016.1176628

Cited by 8 publications

(6 citation statements)

References 45 publications

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“…Thus, after 4h10 exposure to pCD, the expression of ARHGAP26 encoding a protein participating in endocytosis and associated with cancer was upregulated, and TRIM16L involved in cell growth, differentiation and pathogenesis, as well as CEBPD encoding the protein involved in immune and inflammatory responses were downregulated, suggesting the potential impacts of these CDs on immunity, surfactant production [26] and lung carcinogenesis [27]. The effects modulated by the 4h50 exposure to pCD were mostly comparable.…”

Section: Discussionmentioning

confidence: 97%

The Differential Effect of Carbon Dots on Gene Expression and DNA Methylation of Human Embryonic Lung Fibroblasts as a Function of Surface Charge and Dose

Šíma

Vrbová

Závodná

et al. 2020

IJMS

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This study presents a toxicological evaluation of two types of carbon dots (CD), similar in size (<10 nm) but differing in surface charge. Whole-genome mRNA and miRNA expression (RNAseq), as well as gene-specific DNA methylation changes, were analyzed in human embryonic lung fibroblasts (HEL 12469) after 4 h and 24 h exposure to concentrations of 10 and 50 µg/mL (for positive charged CD; pCD) or 10 and 100 µg/mL (for negative charged CD, nCD). The results showed a distinct response for the tested nanomaterials (NMs). The exposure to pCD induced the expression of a substantially lower number of mRNAs than those to nCD, with few commonly differentially expressed genes between the two CDs. For both CDs, the number of deregulated mRNAs increased with the dose and exposure time. The pathway analysis revealed a deregulation of processes associated with immune response, tumorigenesis and cell cycle regulation, after exposure to pCD. For nCD treatment, pathways relating to cell proliferation, apoptosis, oxidative stress, gene expression, and cycle regulation were detected. The expression of miRNAs followed a similar pattern: more pronounced changes after nCD exposure and few commonly differentially expressed miRNAs between the two CDs. For both CDs the pathway analysis based on miRNA-mRNA interactions, showed a deregulation of cancer-related pathways, immune processes and processes involved in extracellular matrix interactions. DNA methylation was not affected by exposure to any of the two CDs. In summary, although the tested CDs induced distinct responses on the level of mRNA and miRNA expression, pathway analyses revealed a potential common biological impact of both NMs independent of their surface charge.

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Section: Discussionmentioning

confidence: 97%

The Differential Effect of Carbon Dots on Gene Expression and DNA Methylation of Human Embryonic Lung Fibroblasts as a Function of Surface Charge and Dose

Šíma

Vrbová

Závodná

et al. 2020

IJMS

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“…Nie et al studied the malignant transformation of immortalized human bronchial epithelial cells (BEAS-2B) irradiated by 0.25 Gy α-particles using miRNA-mRNA networks. Sixty-eight miRNAs were found to be dysregulated, among which miR-107 and miR-494 were predicted to play a role in α-particles-mediated cellular malignant transformation processes by bioinformatics analysis [ 82 ].…”

Section: Mirnas Involved In the Biological Responses To Space Radimentioning

confidence: 99%

“…This suggests that we should consider radiation type, dose, biological samples, as well as sample collection time comprehensively when designing space radiation-related miRNA experiments. In addition, we note that both miR-150-5p and miR-342-3p are down-regulated in blood samples of different mouse models (C57BL/6 or Kunming mice) at 24 h after exposed to different radiation (0.5 Gy iron or carbon ions) [ 80 , 82 ], implying their important regulatory roles in biological effects of heavy ion radiation. Although a large number of miRNAs have been identified to be involved in the responses to space radiation, few functional experiments were carried out.…”

Section: Mirnas Involved In the Biological Responses To Space Radimentioning

confidence: 99%

MicroRNAs Responding to Space Radiation

Yan

Zhang

Zhou

et al. 2020

IJMS

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High-energy and high-atom-number (HZE) space radiation poses an inevitable potential threat to astronauts on deep space exploration missions. Compared with low-LET radiation, high-energy and high-LET radiation in space is more efficient in inducing clustered DNA damage with more serious biological consequences, such as carcinogenesis, central nervous system injury and degenerative disease. Space radiation also causes epigenetic changes in addition to inducing damage at the DNA level. Considering the important roles of microRNAs in the regulation of biological responses of radiation, we systematically reviewed both expression profiling and functional studies relating to microRNAs responding to space radiation as well as to space compound environment. Finally, the directions for improvement of the research related to microRNAs responding to space radiation are proposed. A better understanding of the functions and underlying mechanisms of the microRNAs responding to space radiation is of significance to both space radiation risk assessment and therapy development for lesions caused by space radiation.

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“…The lung and bronchus are the target organs of radon exposure. Preliminary studies in our laboratory found that radon exposure can cause severe damage of mouse lung tissue, and can also cause signi cant changes in mitochondria (Nie et al 2016, Yoshida et al 2011). The result showed that mitochondria should be play an important role in radon-induced lung cancer.…”

Section: Introductionmentioning

confidence: 99%

NF-κB target TFAM to modulate mtDNA copies involved in lung injury of mice induced by radon

Cai

Pei

Jiang

et al. 2023

Preprint

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Radon is the second causative agent of lung cancer after cigarette smoke, it has been identified as a class I carcinogen. However, the exact mechanism of lung cancer caused by radon is still unclear. To examine the underlying mechanism of radon-induced lung injury, a combination of dose- and time-dependent toxic effects in vivo and vitro, NF-κB/TFAM/mtDNA pathway was employed. Radon-induced toxicity occurred in a dose- and time-dependent manners and was characterized by inflammatory cell infiltration, the alveolar septum thickened and the alveolar wall ruptured, moreover, TFAM, NF-κB p65, COXⅡ, ROS and mtDNA signaling pathways were the vital steps in radon-induced pulmonary toxicity. Finally, mitochondrial was identified as a potential target organelle for the further explore of radon-induced lung cancer.

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Analysis of the miRNA–mRNA networks in malignant transformation BEAS-2B cells induced by alpha-particles

Cited by 8 publications

References 45 publications

The Differential Effect of Carbon Dots on Gene Expression and DNA Methylation of Human Embryonic Lung Fibroblasts as a Function of Surface Charge and Dose

The Differential Effect of Carbon Dots on Gene Expression and DNA Methylation of Human Embryonic Lung Fibroblasts as a Function of Surface Charge and Dose

MicroRNAs Responding to Space Radiation

NF-κB target TFAM to modulate mtDNA copies involved in lung injury of mice induced by radon

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