INFLAMMATION AND EPITHELIAL TRANSITION - THE CELLS OF LUNG INFECTIONS, STRUCTURAL AND ADENOIDS

Microenvironment within the tumor and inflammatory cells and their influence secretomes
Nearly all aspects of cancer development (123). The role of chronic inflammation In carcinogenesis is well documented (161-166), such that recently Montavani He suggested that inflammation is a hallmark of cancer and the seventh (167.168). And micro pneumonia caused by tobacco and, in particular, represents Unique to the medium in which carcinogenesis proceeds in complicity with the environment The cells of lung infections, structural and adenoids. Diseases associated with pulmonary disease With increased risk of lung cancer and COPD is characterized IPF, through the many Done and inflammation (169-171). Among the cytokines and growth factors And released mediators in this disease of the lungs and growth in the tumor microenvironment Interleukin-1 beta (IL - 1B), PGE2, and transforming growth factor beta (TGF - b) have properties that prevent harmful both a cell-mediated Immune response against tumor antigens and promote EMT (30, 172-175).
Progress in the field of risk assessment plays a key role in the development of preventive measures Measures. For example, a disease long associated with the risk of lung cancer
(176-178), and recent studies confirm the role of inflammation as Middle of the road capacity audience in the pathogenesis of lung cancer and disease (123179180), and this raises the interesting possibility that is used to reduce agents Patients suffering from chronic inflammation and help prevent lung cancer. To For example, one cohort study have suggested that inhaled corticosteroids may You have a role in preventing lung cancer in patients suffering from this disease (181). Through the study of Another group at high risk for lung cancer - current and former smokers - X Estimates emphysema and spirometric assessment of airflow obstruction and Associated with risk of lung cancer in the population, and provide clinical potential Imaging parameters for assessing the risk of lung cancer (182). Such assessments The measures of attention and appropriate preventive and chemical potential
People who need it most. While the mechanisms linking chronic inflammation and lung cancer are not Determined in a recent version of Houghton et al. Discusses the role of bronchial Stem cells (BASC) (179, 183). This led to a chronic inflammation BASCs quiet to reproduce uncontrollably, which can lead to Top of cancer because of carcinogens the typical rich-inflammatory COPD. In fact, cells BASC not lead to lung cancer in a mouse Model K - Ras-induced malignancy (183). Adair - Kirk et al. Proposal for other mechanisms,
Including the activation of proinflammatory cytokines began waterfall With the inflammasome '"(180, 184) and the expression of proinflammatory genes Induced retinal endoplasmic (ER) revealed the tension caused by the protein Response (UPR) (180, 185). Increase the expression of ER protein identification The stress and the UPR is a mechanism not previously described to begin Inflammatory response to cigarette smoke on lung epithelial cells. Discovery This lining of the lung responds to cigarette smoke in monitoring UPR And antioxidants that cytokine gene expression suggests that efforts should be made
Manufacturers to identify clinically useful lung epithelial stress. Sin and colleagues Recently reported that the protein associated with surfactant - D (SP - D) is a biomarker COPD lung activity, which is relatively specific (180,186). A retrospective analysis Serum samples from the trial of this disease, and low abundance of SP - D During treatment with inhaled corticosteroids increased during the treatment period Recession, making SP - potential marker for lung cancer caused by D cigarette smoke Epithelial cells of strain. In addition, the cast and his colleagues recently discovered that It is expected that the S100 family of proteins associated with inflammation in the survival of large Cohort (n = 196) of patients with NSCLC. By microarray analysis, mRNA expression and high Many S100 proteins, S100A2 in particular, and is associated with poor survival In NSCLC patients surgically  cut, suggesting that these inflammationrelated The proteins are also potential new biomarkers and therapeutic targets In patients with NSCLC. Recent studies shed light on the relationship between inflammation and EMT The development of lung cancer and resistance to therapy (113,172,187). For example, the IL - 1b and PGE2 is able to reduce E - cadherin expression and promote EMT. These inflammatory mediators reach the organization of zinc finger E - connection box Suppressor E-cadherin transcription, including Zeb1, snails, and the league, so Undergoing EMT (113, 172, 175). High levels of snails are present in both human
Lung cancer and premalignant and overexpression increases the helix Phenomena in different malignant human cell lines and immortalized in NSCLC Bronchial epithelial cell lines (188,189). The factors that play a role through the satisfactory Spectrum of carcinogenesis - from pre-malignancy in advanced disease - a Original as potential targets for treatment. For example, 30% of patients with lung cancer After eradication of the disease in the early development of relapse. In this population, with a view And can treat cancer patients that potentially any residual factors, they are already While the prevention of cancer are at risk from developing countries. EMT requires changes in cell morphology, adhesion and migration (190). The result of these cellular changes in the variable expression of the proteins that are EMT The signs. And down - cadherin, which allows a reduction of cell-cell adhesion-and Promote the migration of cells is a characteristic of EMT. Dohadwala and colleagues Already shown a list of COX - 2 - dependent transcription of E - cadherin
Cellular expression and assembly in NSCLC and no correlation between COX - 2, and E - cadherin, ZEB1 and E - cadherin (172). COX - 2 and PGE2 Expression resulted in a significant reduction of E - cadherin transcription through suppressing ZEB1 and snail. Led to inhibition of COX - 2 to save the E - cadherin Of expression. It may, therefore, treatments that aim to COX-path reduces the tendency For a malignant tumor in NSCLC, preventing the stimulation of PGE2-mediated E - cadherin repression of transcription. This way to set the new transcript The organization of E-cadherin in NSCLC has important implications for chemoprevention Treatment of NSCLC and use of COX - 2 in combination with other And agents. For example, the recent E - cadherin expression in NSCLC involved As an indication of the sensitivity of the EGFR tyrosine kinase inhibitors (191-193). Consistent and low serum
E - cadherin levels associated with response to combination treatment with erlotinib and
Celecoxib in patients with NSCLC (194). Expression through E - cadherin helps COX inhibitors may be - 2 increased sensitivity EGFR TKI therapy (139). Recent work from the laboratory and Weinberg suggest a direct link between the EMT and Get the characteristics of epithelial cells (195). Thus, in the pathogenesis of lung cancer, Inflammation can promote stem cell like properties through EMT-dependent events. As And the involvement of EMT by changes in the metastatic process and the work of Mani Colleagues suggest that the genetic program of EMT may also regulate activities in the early Carcinogenesis, hence the involvement of the lung inflammatory environment in each of the Lung cancer metastatic to start and progress, as summarized recently by Sanchez Garcia (195,196). Development of mouse models of EMT, and identify the self- Inhibitors of AA, and for the development of synthetic inhibitors is now a strong focus Since the investigation of E – cadherin transcriptional suppressor may be located at the intersection of Inflammation, EMT, and the development of lung cancer.