ABSTRACT
AIM:To explore the expression level of long non-coding RNA(lncRNA)myocardial infarction-as-sociated transcript(MIAT)in the tissues and cells of non-small-cell lung carcinoma(NSCLC), and to investigate the effect of MIAT on the function of NSCLC cell line.METHODS:Bioinformatic data in microarray dataset GSE19804 from Gene Expression Omnibus(GEO)were collected for analyzing the difference expression of MIAT between NSCLC tissues and normal lung tissues.Clinical and prognostic data in microarray dataset GSE 30219 from GEO were also collected for an-alyzing the correlation between the expression level of MIAT and the survival time of NSCLC patients.qPCR was applied to detect the expression of MIAT in 25 paired tumor tissues and corresponding adjacent normal tissues,normal lung epithelial HBE cell line and NSCLC A549,NCI-H266 and NCI-H1299 cell lines.The specific small interfering RNA for MIAT(si-MIAT group)or negative control sequence(si-NC group)was transfected into A549 cells,and flow cytometry,colony for-mation experiment and CCK-8 assay were employed to detect the proliferation of the cells in the 2 groups.The expression levels of cyclin D1 and cyclin-dependent kinase inhibitor 1A(CDKN1A)in the 2 groups were determined by qPCR and Western blot.RESULTS:In the GEO dataset GSE19804,the expression of MIAT in NSCLC tissues was significantly ele-vated compared with normal lung tissues(P<0.05).In the GEO dataset GSE30219,the overall survival time was signifi-cantly shorter in the patients with high expression of MIAT than the patients with low expression of MIAT(P<0.05).Fur-thermore,the levels of MIAT in both NSCLC tissues and cells were higher than those in adjacent normal tissues and normal cells(P<0.05).Compared with si-NC group,lower MIAT level,cell viability and cell colony number in si-MIAT group with statistical significance were observed(P<0.05).Meanwhile, compared with si-NC group, the expression of cyclin D1 in si-MIAT group was significantly decreased(P<0.05),and inversely,the expression of CDKN1A in si-MIAT group was significantly increased(P<0.05).CONCLUSION:There is high expression of MIAT in NSCLC tissues and NSCLC cells,and knockdown of MIAT expression inhibits NSCLC cell proliferation, which provides a potential target of targeted therapy for NSCLC.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the mechanism of tanshinol on alleviate the inflammatory injury of lung tissue in rat hepatopulmonary syndrome (HPS).</p><p><b>METHODS</b>SD rats were randomly divided into normal control group (n = 8), hepatopulmonary syndrome (HPS) group (n = 11) and tanshinol intervention group (n = 9). HE staining was used to observe the histopathology changes of pulmonary and hepatic tissues, and to count the number of macrophages in lung tissues. The activity of alanine transferase (ALT) and concentrations of endotoxin, tumor necrosis factor-a (TNF-alpha) and homocystein (Hcy) in plasma were detected. The concentrations of TNF-alpha, nitric oxide (NO) and malondialdehyde (MDA) and the activity of inducible nitric oxide synthase (iNOS) in the lung tissues were measured, respectively.</p><p><b>RESULTS</b>Thickened alveolar septum and increased macrophages were observed in lungs in HPS rat. After administered with tanshinol, the pulmonary pathological changes were alleviated and the number of macrophages in lung tissue was decreased compared with HPS group. The activity of ALT and the concentrations of endotoxin, TNF-alpha and Hcy in plasma ,and TNF-alpha, iNOS, NO and MDA in lung tissue in HPS group were higher than those of normal control group; meanwhile, those tanshinol group were less those that of HPS group.</p><p><b>CONCLUSION</b>Tanshinol may play an important role in delaying the development of HPS through protecting liver or directly antagonizing the effect of intestinal endotoxemia so as to alleviate the inflammatory reaction in lung tissue.</p>