28 research outputs found

    Investigation of miR221 and miR222 as biomarkers in non-small cell lung cancer

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    Background/Aim: MicroRNAs (miRNA) are a class of small non-coding RNAs of 18-25 nucleotides, which regulate gene expression at the post-transcriptional level by disrupting or blocking translation of messenger RNA targets. Non-small cell lung cancer (NSCLC) represents approximately 85% of all lung cancers. Early and accurate diagnosis of the disease affects the probability of success of treatment. The purpose of this study was to investigate the expression levels of serum specific miRNA221 and miRNA222 as a biomarker in NSCLC. Materials and Methods: Thirty-two NSCLC cases and 30 healthy control cases that were diagnosed at Istanbul Yedikule Chest Diseases and Thoracic Surgery Training Hospital were included in this study. miRNAs were detected using miRNAspecific quantitative real-time-PCR. The relative expression of miRNAs was calculated using the 2-ccCt method. Results: miR221 and miR222 showed 1.46 and 1.63-fold higher expression in the samples from patients with NSCLC compared to controls, and the difference of expression was statistically significant for miR221 (p=0.000095) but not for miR222 (p=0.084470). In the presence of metastasis in NSCLC patients, miR221 levels were 2.33-fold higher compared to non-metastatic cases (p=0.014), and those of miR221 and miR222 were expressed 1.44 and 1.52-fold higher, respectively, in advanced stage compared to early stage (p=0.000387, p=0.000302). Conclusion: The levels of miR221 and miR222 in the serum of patients could be used as biomarkers for the diagnosis, treatment, and prognosis of NSCLC.Istanbul Universit

    Investigation of NF-kappa B1 and NF-kappa BIA gene polymorphism in non-small cell lung cancer

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    Lung cancer is a complex, multifactorial disease which is the leading cause of cancer death in both men and women. NF-B is a transcription factor which is known to affect the expression of more than 150 genes related to inflammation, lymphocyte activation, cell proliferation, differentiation, and apoptosis, as well as contributing to cell apoptosis and survival. However, NF-BIA (IB?) is the inhibitor of the transcription factor. The -94ins/delATTG polymorphism of the NF-B1 gene promoter region which causes a functional effect and NF-BIA 3'UTR A › G polymorphism has been shown to be related to various inflammatory diseases and cancer. Ninety-five NSCLC patients and 99 healthy controls were included in study. The NF-B1 -94ins/delATTG and NF-BIA 3'UTR A › G polymorphism have been studied by using PCR-RFLP method. It was found that the NF-B1 -94ins/delATTG DD genotype and D allele frequencies were higher in patients than healthy controls and the presence of the DD genotype has a 3.5-fold increased risk of the disease (P: 0.014). This study is the first to investigate the NF-B1 -94ins/delATTG and NF-BIA 3'UTR A › G polymorphism together in the Turkish population. According to the results, the NF-B1 -94ins/del ATTG promoter polymorphism may have a role in lung carcinogenesis and prognosis

    The significance of HSP90AA1, HSP90AB1 and HSP90B1 gene polymorphisms in a Turkish population with non-small cell lung cancer

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    Background/Aim: Heat-shock proteins (HSPs) are molecular chaperones which modify the structures and interactions of other proteins. The aim of our study was to investigate HSP90AA1, HSP90AB1 and HSP90B1 gene polymorphisms in patients with non-small cell lung cancer (NSCLC). Materials and Methods: Ninety-seven patients with NSCLC and 97 healthy controls were included in the study. Real-time polymerase chain reaction was used for genotyping. Results: The frequency of mutant CC genotype for HSP90AA1 (rs4947C/T), mutant AA genotype for HSP90AB1 (rs13296A/G) and mutant CC genotype for HSP90B1 (rs2070908 C/G) was significantly higher in the patient group than in controls (p=0.019, p=0.004 and p=0.036, respectively). The frequency of patients with homozygote mutant allele was also significantly higher than that of controls and possessing of the mutant genotype increased the risk for disease by approximately 2.9, 4.8, 1.9 for HSP90AA1, HSP90AB1 and HSP90B1, respectively. The present study appears to be the first of its kind to report data on these gene polymorphisms in patients with NSCLC in the Turkish population.Istanbul Universit

    Lack of association between increased mitochondrial DNA(4977) deletion and ATP levels of sputum cells from chronic obstructive pulmonary disease patients versus healthy smokers

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    WOS: 000397858400027PubMed ID: 26713688In this study we looked at smokers with and without chronic obstructive pulmonary disease (COPD) patients in order to evaluate the incidence of 4977 base pair (bp) mtDNA (mtDNA(4977)) deletion and mtDNA copy number in sputum cells and in peripheral blood leukocytes (PBLs) in relation to mitochondrial function and oxidative stress status. Twenty-five COPD patients who were current smokers, 22 smokers and 23 healthy nonsmokers (for only PBLs studies) participated in this study. The 4977-bp deletion was detected in all examined samples within 40 cyles of PCR amplification, using a quantitative real time PCR. The frequency of the mtDNA(4977) was significantly higher in the sputum cells of patients with COPD compared to smokers without COPD (p<0.0001). This difference was not observed in PBLs. Levels of cellular oxidative stress were significantly higher in the sputum cells of subjects with COPD than in the smoker group. However, mtDNA copy number, mitochondrial membrane potential (Delta Psi m) and cellular ATP levels in PBLs and sputum cells were not significantly different between the studied groups. The Pearson analysis revealed no correlations between the accumulation of mtDNA(4977), and intracellular ATP content and Delta Psi m values of the sputum cells, although there was a positive correlation between the increase in the percentage of deleted mtDNA(4977) and the levels of cellular oxidative stress in COPD patients (r = 0.80, p<0.0001). Our studies may suggest that the accumulation of mtDNA(4977) in the sputum cells of smokers with COPD does not seem to have an important impact on mitochondrial dysfunction in relation to ATP production and Delta Psi m when compared to those of healthy smokers.Research Fund of Istanbul University [T81/12122006]There is no conflict of interest among the author. This work was supported by the Research Fund of Istanbul University (project number: T81/12122006)
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