Related Articles

Functional analysis of DNA methylation in lung cancer.

Eur Rev Med Pharmacol Sci. 2013 May;17(9):1191-7

Authors: Li B, Lu Q, Song ZG, Yang L, Jin H, Li ZG, Zhao TJ, Bai YF, Zhu J, Chen HZ, Xu ZY

Abstract
OBJECTIVES: We aimed to explore the DNA methylation difference between lung cancer samples and non-cancer lung samples, and to investigate the role of DNA methylation in the mechanism of lung cancer development. Besides, we analyzed the transcriptional regulation network of DNA methylation and the miRNAs regulated by DNA methylation. This study provides a framework for DNA methylation in other tumors or diseases.
MATERIALS AND METHODS: DNA methylation and gene expression profiles used were obtained from Gene Expression Omnibus. Firstly, we identified differentially methylated genes (DMGs) by Student's t-test. Then we detected the biological processes and pathways changed in lung cancer by Gene Ontology (GO) and KEGG pathway enrichment analysis. The transcriptional factors in differential genes were identified and the microRNAs regulated by them were also obtained in TransmiR.
RESULTS: We obtained 108 DMGs between lung cancer samples and non-cancer samples. Besides development related biological processes and pathways were dramatically disordered. For the DMGs, we identified 11 transcriptional factors regulating them. Moreover, we screened out 21 relationships between DMGs and their transcriptional targets. Five microRNAs are reported to be regulated by DNA methylation genes. Finally a regulation network of DNA methylation was constructed.
CONCLUSIONS: DNA methylation participates in carcinogenesis at the transcriptional and post-transcriptional level. Aberrant DNA methylation will prevent its binding with the upstream regulatory proteins, inhibit the function of downstream target genes and regulate the expression of downstream miRNA, and consequently affect cell development, immuneresponse and apoptosis.

PMID: 23690188 [PubMed - in process]

Related Articles

Inflammatory signalings involved in airway and pulmonary diseases.

Mediators Inflamm. 2013;2013:791231

Authors: Lee IT, Yang CM

Abstract
In respiratory diseases, there is an increased expression of multiple inflammatory proteins in the respiratory tract, including cytokines, chemokines, and adhesion molecules. Chemokines have been shown to regulate inflammation and immune cell differentiation. Moreover, many of the known inflammatory target proteins, such as matrix metalloproteinase-9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2), are associated with airway and lung inflammation in response to various stimuli. Injuriously environmental stimuli can access the lung through either the airways or the pulmonary and systemic circulations. The time course and intensity of responses by resident and circulating cells may be regulated by various inflammatory signalings, including Src family kinases (SFKs), protein kinase C (PKC), growth factor tyrosine kinase receptors, nicotinamide adenine dinucleotide phosphate (NADPH)/reactive oxygen species (ROS), PI3K/Akt, MAPKs, nuclear factor-kappa B (NF- κ B), activator protein-1 (AP-1), and other signaling molecules. These signaling molecules regulate both key inflammatory signaling transduction pathways and target proteins involved in airway and lung inflammation. Here, we discuss the mechanisms involved in the expression of inflammatory target proteins associated with the respiratory diseases. Knowledge of the mechanisms of inflammation regulation could lead to the pharmacological manipulation of anti-inflammatory drugs in the respiratory diseases.

PMID: 23690670 [PubMed - in process]

Plant-Derived Foods For The Attenuation Of Allergic Airway Inflammation.

Curr Pharm Des. 2013 May 17;

Authors: Nyanhanda T, Gould EM, Hurst RD

Abstract
Asthma is an allergy-mediated inflammatory disease characterised by infiltration of the airway with mast cells, lymphocytes, and eosinophils. The disease is induced by co-ordination of T-helper cell type 2 (Th2) cytokines and inflammatory signal molecules. Fruits and vegetables are a rich source of polyphenolic bioactive compounds, which have been observed to have health-promoting properties when consumed by humans. In particular, fruit-derived proanthocyanins and anthocyanins have been found to attenuate lung inflammation. Epidemiological studies have revealed correlations between fruit consumption and a lower prevalence of respiratory symptoms and lower incidence of non-specific lung diseases. In this review we summarise the current understanding of the pathophysiologic mechanism(s) involved in the development of allergic airway disease. We also review evidence of the beneficial effects of plant-derived foods, their components and metabolites in allergic airway inflammation arising from in vitro and rodent studies, epidemiological studies and human intervention trials. The mechanism, biological relevance and functional benefits, such as immune modulation (e.g. reduction in cytokine and eotaxin production), antioxidant ability, tissue remodelling and tight junction function are also discussed.

PMID: 23701570 [PubMed - as supplied by publisher]