RESUMO
BackgroundSince the role of long non-coding RNA (lncRNA) HOTAIR is yet to be established in non-small cell lung cancer (NSCLC), we tried to explore the expression of lncRNA HOTAIR in NSCLC and evaluate the correlation between the combined detection of lncRNA HOTAIR and routine tumour markers and the pathological staging of lung cancer.MethodsThis study prospectively included 148 patients with NSCLC selected from our hospital from January 2017 to September 2020 as the lung cancer group, and 148 healthy volunteers who referred for physical examination were selected as the control group. Fluorescence in situ hybridisation was used to detect the expression of lncRNA HOTAIR in the cancerous tissues and adjacent tissues of lung cancer patients; the immunofluorescence method was used to detect the serum NSE, CEA and CYFRA21-1 levels of the two groups of testers. Correlation analysis was used to evaluate any relation between cancer staging and markers. In addition, ROC curve analysis was used to estimate sensitivity, specificity, positive predictive value, and negative predictive value.ResultsThe expression of lncRNA HOTAIR in lung cancer tissues was higher than control or surrounding tissue (p < 0.05). Also, high levels of NSE, CEA and CYFRA21-1 were observed in lung cancer group (p < 0.05). In both N and T stage, the expression of lncRNA HOTAIR combined with NSE, CEA and CYFRA21-1 levels increased with the increase in the number of stages (p < 0.05). The results of single factor analysis showed that NSE, CEA, CYFRA21-1 and lncRNA HOTAIR all have appropriate diagnostic value for detecting lung cancer (specificity of 92.6, 91.5, 90.6, 86.9%, respectively and the sensitivity of 61.3, 62.9, 55.4, 52.3%, respectively).ConclusionLncRNA HOTAIR is a novel diagnostic test with high diagnostic value for detecting of pathological staging of NSCLC; however, the diagnostic accuracy of lncRNA HOTAIR is not higher than other tumour biomarkers.
Assuntos
Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , RNA Longo não Codificante , Antígenos de Neoplasias/genética , Biomarcadores Tumorais/genética , Antígeno Carcinoembrionário , Carcinoma Pulmonar de Células não Pequenas/diagnóstico , Carcinoma Pulmonar de Células não Pequenas/genética , Humanos , Queratina-19 , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/genética , RNA Longo não Codificante/genéticaRESUMO
A porcine model was produced to study the pathophysiology of congenital heart defect (CHD) with decreased pulmonary blood flow. Twenty piglets (1-2 months) were randomly divided as mild to moderate stenosis/T(1) group (n = 7) in which artificial atrial septal defect (ASD) with pulmonary artery banding generated a systolic pressure gradient of 20-30 mmHg; severe stenosis/T group (n = 7) group with a systolic pressure gradient of ≥30-50 mmHg; and controls/C group (n = 6) underwent sham surgery. At 1 month postoperatively, 64-slice computed tomography (CT) was performed. At 2 months, left-chest surgery was performed to measure ASD diameter, arterial blood gas, hemoglobin, and Trans-PABP. Our data show successful establishment of porcine CHD model. ASDs in T(1)/T(2) groups were 8.0 ± 0.5/8.9 ± 1.4 mm, respectively. Trans-PABP showed that the pressure increase in T(2) was higher (P < 0.01) than in T(1) group. Arterial blood PaO(2) and SaO(2) of T(1/)T(2) groups were significantly lower than controls. AoD was significantly lower in T(1) than in C group. Balloon dilation was significantly lower than AoD in T(1)/T(2) groups. Besides, one animal in T(1), two animals in T(2) ,and one animal in C group died. We conclude that ASD with pulmonary artery banding is a successful intervention to establish such a model, and our findings may influence the treatment of patients with similar heart disease.