Analysis of plasma microRNA expression profiles revealed different cancer susceptibility in healthy young adult smokers and middle-aged smokers

Shi, Bing; Gao, Hongmin; Zhang, Tianyang; Cui, Qinghua

doi:10.18632/oncotarget.7866

Cited by 20 publications

(13 citation statements)

References 30 publications

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“…Interestingly, nicotine shows an ability of decreasing ACE2 expression, suggesting a possible role of anti-2019-nCoV. This finding may be consistent with our previous report that smoking-inhibited miRNAs are significantly associated with SARS [27]. For the biologics, previous reports supported the prediction for lipopolysaccharide [28].…”

Section: The Jmap Agents That Decrease Ace2 Expressionsupporting

confidence: 90%

Possible Inhibitors of ACE2, the Receptor of 2019-nCoV

Cui¹,

Huang²,

X³

et al. 2020

Preprint

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Most recently, an outbreak of severe pneumonia caused by the infection of 2019-nCoV, a novel coronavirus first identified in Wuhan, China, imposes serious threats to public health. Many important aspects about 2019-nCoV remain largely unknown, among which, the limitation of antiviral therapies represents one of the most critical problems. More recently, it was confirmed that human ACE2 is the receptor for the entry of 2019-nCoV into lower respiratory tract epithelial cells. Give this observation, it is thus expected that the virus could be inhibited if we decrease the expression of ACE2. Here by screening two databases, Connectivity Map (CMap) and our JeaMoon Map (JMap), we identified a number of candidate agents that decrease ACE2 expression. CMap analysis identified 5 compounds, among which, Azathioprine is a possible therapeutic strategy for anti-2019-nCoV. Moreover, JMap analysis revealed a number of comounds, biologics, and traditional Chinese medicine, among which, Andrographis, Urtica, Sambucus, Astragalus, valproic acid, butyrate, and epoxomicin represent the most significant and possible strategies for anti-2019-nCoV therapies. This study provides a number of clues and possible therapeutic strategies for 2019-nCoV prevention and treatment.

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Section: The Jmap Agents That Decrease Ace2 Expressionsupporting

confidence: 90%

Possible Inhibitors of ACE2, the Receptor of 2019-nCoV

Cui¹,

Huang²,

X³

et al. 2020

Preprint

Self Cite

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“…To our knowledge, this study is the first study to demonstrate that miR-34b-5p may be involved in the pathogenesis of ALV-J, as it appears to affect many aspects of cancer biology, such as cell proliferationand cell cycle progression. We further investigated the biological functions of miR-34b-5p using an overexpression experiment (Zhao et al, 2015 ; Shi B. et al, 2016 ). The functional investigation demonstrated that ectopic expression of miR-34b-5p could accelerate cell proliferation and migration in ALV-J-infected cells.…”

Section: Discussionmentioning

confidence: 99%

MiR-34b-5p Suppresses Melanoma Differentiation-Associated Gene 5 (MDA5) Signaling Pathway to Promote Avian Leukosis Virus Subgroup J (ALV-J)-Infected Cells Proliferaction and ALV-J Replication

Luo

et al. 2017

Front. Cell. Infect. Microbiol.

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Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that has a similar replication cycle to multiple viruses and therefore can be used as a model system for viral entry into host cells. However, there are few reports on the genes or microRNAs (miRNAs) that are responsible for the replication of ALV-J. Our previous miRNA and RNA sequencing data showed that the expression of miR-34b-5p was significantly upregulated in ALV-J-infected chicken spleens compared to non-infected chicken spleens, but melanoma differentiation-associated gene 5 (MDA5) had the opposite expression pattern. In this study, a dual-luciferase reporter assay showed that MDA5 is a direct target of miR-34b-5p. In vitro, overexpression of miR-34b-5p accelerated the proliferation of ALV-J-infected cells by inducing the progression from G2 to S phase and it promoted cell migration. Ectopic expression of MDA5 inhibited ALV-J-infected cell proliferation, the cell cycle and cell migration, and knockdown of MDA5 promoted proliferation, the cell cycle and migration. In addition, during ALV-J infections, MDA5 can detect virus invasion and it triggers the MDA5 signaling pathway. MDA5 overexpression can activate the MDA5 signaling pathway, and thus it can inhibit the mRNA and protein expression of the ALV-J env gene and it can suppress virion secretion. In contrast, in response to the knockdown of MDA5 by small interfering RNA (siRNA) or an miR-34b-5p mimic, genes in the MDA5 signaling pathway were significantly downregulated (P < 0.05), but the mRNA and protein expression of ALV-J env and the sample-to-positive ratio of virion in the supernatants were increased. This indicates that miR-34b-5p is able to trigger the MDA5 signaling pathway and affect ALV-J infections. Together, these results suggest that miR-34b-5p targets MDA5 to accelerate the proliferation and migration of ALV-J-infected cells, and it promotes ALV-J replication, via the MDA5 signaling pathway.

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“…It was shown that cigarette smoking can change microRNA profile in many human organs and induces the change of plasma miRNA expression profiles in healthy subjects. Using microarray, Shi and co-authors [ 82 ] identified 24 up-regulated and 11 down-regulated plasma miRNAs in young healthy smokers. The authors concluded that the changes in miRNA expression profile caused by smoking can be viewed as risk factors for cancers (especially leukemia and lymphoma), cardiovascular disease, and metabolic syndrome in young adult smokers.…”

Section: Effects Of Xenobiotics On Mirna Expressionmentioning

confidence: 99%

Regulatory mechanisms of microRNA expression

2016

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MicroRNAs (miRs, miRNAs) are small molecules of 18–22 nucleotides that serve as important regulators of gene expression at the post-transcriptional level. One of the mechanisms through which miRNAs regulate gene expression involves the interaction of their “seed” sequences primarily with 3′-end and more rarely with 5′-end, of mRNA transcribed from target genes. Numerous studies over the past decade have been devoted to quantitative and qualitative assessment of miRNAs expression and have shown remarkable changes in miRNA expression profiles in various diseases. Thus, profiling of miRNA expression can be an important tool for diagnostics and treatment of disease. However, less attention has been paid towards understanding the underlying reasons for changes in miRNA expression, especially in cancer cells. The purpose of this review is to analyze and systematize current data that explains reasons for changes in the expression of miRNAs. The review will cover both transcriptional (changes in gene expression and promoter hypermethylation) and post-transcriptional (changes in miRNA processing) mechanisms of regulation of miRNA expression, as well as effects of endogenous (hormones, cytokines) and exogenous (xenobiotics) compounds on the miRNA expression. The review will summarize the complex multilevel regulation of miRNA expression, in relation to cell type, physiological state of the body and various external factors.

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Analysis of plasma microRNA expression profiles revealed different cancer susceptibility in healthy young adult smokers and middle-aged smokers

Cited by 20 publications

References 30 publications

Possible Inhibitors of ACE2, the Receptor of 2019-nCoV

Possible Inhibitors of ACE2, the Receptor of 2019-nCoV

MiR-34b-5p Suppresses Melanoma Differentiation-Associated Gene 5 (MDA5) Signaling Pathway to Promote Avian Leukosis Virus Subgroup J (ALV-J)-Infected Cells Proliferaction and ALV-J Replication

Regulatory mechanisms of microRNA expression

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