Hypermethylation of Anti-oncogenic MicroRNA 7 is Increased in Emphysema Patients

Rosas-Alonso, Rocío; Galera, Raúl; Sánchez-Pascuala, Joan José; Casitas, Raquel; Burdiel, Miranda; Martínez‐Cerón, Elisabet; Vera, Olga; Rodriguez-Antolín, Carlos; Pernía, Olga; Castro, Javier de; García‐Río, Francisco; Ibáñez-de-Cáceres, Inmaculada

doi:10.1016/j.arbr.2019.10.019

Cited by 5 publications

(2 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lusk et al (47) established the different genetic profiles of patients with LC by reference to the specific emphysema subphenotype, while activation of the ERK (extracellular signal-regulated kinase) oncogene has also been described as a nicotinic acetylcholine receptor (48). Rosas-Alonso et al (49) analysed the effect of hypermethylation of microARN 7 (miR-7) (anti-oncogenic action) in a prospective study that included 30 smokers without airflow obstruction and 136 patients with COPD without evidence of LC. They observed a higher miR-7 hypermethylation value in patients with COPD and emphysema (27.1%±10.2%), as compared to patients with exacerbator phenotype (19.4%±9.9%, P=0.004), chronic bronchitis (17.3%±9%, P=0.002) or asthma-COPD overlap (ACO) (16%±7.2%, P=0.01), after adjustment for clinical parameters and differences between phenotypes.…”

Section: Emphysema and Lc: Mechanisms Implicatedmentioning

confidence: 99%

Lung emphysema and lung cancer: what do we know about it?

et al. 2020

View full text Add to dashboard Cite

Emphysema and lung cancer (LC) are two diseases which share common risk factors, e.g., smoking. In recent years, many studies have sought to analyse this association. By way of illustration, we conducted a review of the scientific literature of the studies published to date, whose main designated aim was to demonstrate the relationship between emphysema and LC, and this association's influence on the histology, prognosis and molecular mechanisms responsible. We included over 40 studies (ranging from case-control and cohort studies to systematic reviews and meta-analyses), which highlight the association between emphysema and LC, independently of smoking habit. These studies also report a possible influence on histology, with adenocarcinoma being the most frequent lineage, and an association with poor prognosis, which affects both survival and post-operative complications. Oxidative stress, which generates chronic inflammatory status as well as the presence of certain polymorphisms in various genes (CYP1A1, TERT, CLPTM1L, ERK), gives rise-in the case of patients with emphysema-to alteration of cellular repair mechanisms, which in turn favours the proliferation of neoplastic epithelial cells responsible for the origin of LC.

show abstract

Section: Emphysema and Lc: Mechanisms Implicatedmentioning

confidence: 99%

Lung emphysema and lung cancer: what do we know about it?

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Low blood eosinophils, elevated plasmin–mediated degradation of cross-linked fibrin, and hypermethylation of microRNA-7 are regarded as the features of emphysematous phenotype ( Papaioannou et al, 2017 ; Manon-Jensen et al, 2019 ; Rosas-Alonso et al, 2020) , but their potential to serve as prognostic biomarkers needs further validation. Moreover, the underlying molecular mechanism of COPD emphysematous phenotype remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Identification of Proteomic Signatures in Chronic Obstructive Pulmonary Disease Emphysematous Phenotype

Bai

Rui

Wang

et al. 2021

Front. Mol. Biosci.

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is a highly heterogeneous disease. Emphysematous phenotype is the most common and critical phenotype, which is characterized by progressive lung destruction and poor prognosis. However, the underlying mechanism of this structural damage has not been completely elucidated. A total of 12 patients with COPD emphysematous phenotype (COPD-E) and nine patients with COPD non-emphysematous phenotype (COPD-NE) were enrolled to determine differences in differential abundant protein (DAP) expression between both groups. Quantitative tandem mass tag–based proteomics was performed on lung tissue samples of all patients. A total of 29 and 15 lung tissue samples from patients in COPD-E and COPD-NE groups, respectively, were used as the validation cohort to verify the proteomic analysis results using western blotting. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted for DAPs. A total of 4,343 proteins were identified, of which 25 were upregulated and 11 were downregulated in the COPD-E group. GO and KEGG analyses showed that wound repair and retinol metabolism–related pathways play an essential role in the molecular mechanism of COPD emphysematous phenotype. Three proteins, namely, KRT17, DHRS9, and FMO3, were selected for validation. While KRT17 and DHRS9 were highly expressed in the lung tissue samples of the COPD-E group, FMO3 expression was not significantly different between both groups. In conclusion, KRT17 and DHRS9 are highly expressed in the lung tissue of patients with COPD emphysematous phenotype. Therefore, these proteins might involve in wound healing and retinol metabolism in patients with emphysematous phenotype and can be used as phenotype-specific markers.

show abstract