Abstract
Lung cancer (LC) risk increases in patients with chronic respiratory diseases (COPD). MicroRNAs and redox imbalance are involved in lung tumorigenesis in COPD patients. Whether systemic alterations of those events may also take place in LC patients remains unknown. Our objectives were to assess the plasma levels of microRNAs, redox balance, and cytokines in LC patients with/without COPD. MicroRNAs (RT-PCR) involved in LC, oxidized DNA, MDA-protein adducts, GSH, TEAC, VEGF, and TGF-beta (ELISA) were quantified in plasma samples from non-LC controls (n = 45), LC-only patients (n = 32), and LC-COPD patients (n = 91). In LC-COPD patients compared to controls and LC-only, MDA-protein adduct levels increased, while those of GSH decreased, and two patterns of plasma microRNA were detected. In both LC patient groups, miR-451 expression was downregulated, while those of microRNA-let7c were upregulated, and levels of TEAC and TGF-beta increased compared to the controls. Correlations were found between clinical and biological variables. A differential expression profile of microRNAs was detected in patients with LC. Moreover, in LC patients with COPD, plasma oxidative stress levels increased, whereas those of GSH declined. Systemic oxidative and antioxidant markers are differentially expressed in LC patients with respiratory diseases, thus implying its contribution to the pathogenesis of tumorigenesis in these patients.
Highlights
Introduction iationsLung cancer (LC) is still a leading cause of cancer-related mortality worldwide
The proportions of ex-smokers were significantly greater in the LC-chronic obstructive pulmonary disease (COPD) group than in the LC-only group and showed a tendency to be higher than in the control subjects (p = 0.1, Table 2)
The proportions of never smokers were significantly lower in the LC-COPD patients than in the LC-only and the control subjects (Table 2)
Summary
Introduction iationsLung cancer (LC) is still a leading cause of cancer-related mortality worldwide. Several etiologic factors contribute to LC, among which chronic obstructive pulmonary disease (COPD) is a major contributor [1,2,3,4]. In patients with COPD, in emphysema phenotype, LC development was five times greater than in smokers with no COPD [4,5]. Our group and others have demonstrated the implications of relevant biological mechanisms in the increased LC predisposition seen in patients with COPD [6,7,8,9,10,11,12,13]. Adaptation to environmental factors and tumorigenesis are mediated through many different biological events including epigenetics. Epigenetic control of cellular processes includes DNA methylation, histone acetylation and methylation, and chromatin remodeling in tumor development and progression [14].
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