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Chronic obstructive pulmonary disease (COPD) is a common airway disease, and epithelial mesenchymal transition (EMT) is participated in the pathogenesis of COPD. However, the role of CD147 in COPD remains largely unknown. In order to clarify the role of CD147 in EMT induced by cigarette smoke, we established animal and cell model of EMT by mean of cigarette smoke exposure and detected the expressions of CD147 and EMT markers

The present study was carried out to investigate the role of lncRNA TP73-AS1 in non-small cell lung cancer (NSCLC). We found that TP73-AS1 was upregulated in tumor tissues than in non-tumor tissues of NSCLC patients, and high expression levels of TP73-AS1 predicted poor survival. MiR-21 was also upregulated in tumor tissues and positively correlated with TP73-AS1. TP73-AS1 overexpression led to miR-21 upregulation, while miR-21 overexpression failed to affect TP73-AS1. TP73-AS1 and miR-21 overexpression caused the accelerated invasion and migration of NSCLC cells. However, TP73-AS1 overexpression failed to affect cell proliferation. Therefore, TP73-AS1 may upregulate miR-21 to promote NSCLC cell migration and invasion.

Objective The primary aim of our study was to explore the mechanisms through which long non-coding RNA (lncRNA)-mediated sirtuin-1 (SIRT1) signaling regulates type II alveolar epithelial cell (AECII) senescence induced by a cigarette smoke-media suspension (CSM). Methods Pharmacological SIRT1 activation was induced using SRT2104 and senescence-associated lncRNA 1 (SAL-RNA1) was overexpressed. The expression of SIRT1, FOXO3a, p53, p21, MMP-9, and TIMP-1 in different groups was detected by qRT-PCR and Western blotting; the activity of SA-β gal was detected by staining; the binding of SIRT1 to FOXO3a and p53 gene transcription promoters was detected by Chip. Results We found that CSM increased AECII senescence, while SAL-RNA1 overexpression and SIRT1 activation significantly decreased levels of AECII senescence induced by CSM. Using chromatin immunoprecipitation, we found that SIRT1 bound differentially to transcriptional complexes on the FOXO3a and p53 promoters. Conclusion Our results suggested that lncRNA-SAL1-mediated SIRT1 signaling reduces senescence of AECIIs induced by CSM. These findings suggest a new therapeutic target to limit the irreversible apoptosis of lung epithelial cells in COPD patients.

Supplemental material, sj-pdf-4-imr-10.1177_0300060520986049 for Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling by Dong Yuan, Yuanshun Liu, Mengyu Li, Hongbin Zhou, Liming Cao, Xiaoqin Zhang and Yaqing Li in Journal of International Medical Research

Supplemental material, sj-pdf-1-imr-10.1177_0300060520986049 for Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling by Dong Yuan, Yuanshun Liu, Mengyu Li, Hongbin Zhou, Liming Cao, Xiaoqin Zhang and Yaqing Li in Journal of International Medical Research

Supplemental material, sj-pdf-2-imr-10.1177_0300060520986049 for Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling by Dong Yuan, Yuanshun Liu, Mengyu Li, Hongbin Zhou, Liming Cao, Xiaoqin Zhang and Yaqing Li in Journal of International Medical Research

Supplemental material, sj-pdf-3-imr-10.1177_0300060520986049 for Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling by Dong Yuan, Yuanshun Liu, Mengyu Li, Hongbin Zhou, Liming Cao, Xiaoqin Zhang and Yaqing Li in Journal of International Medical Research

Objective: The aim of the study is to evaluate the effects of silencing a disintegrin and metalloproteinase 17 (ADAM17) gene expression by lentivirus‐mediated RNA interference (RNAi) in the gefitinib‐resistant lung adenocarcinoma cells, and then to explore whether the recombinant lentivirus mediated ADAM17 RNAi reversed the acquired resistance of lung adenocarcinoma to gefitinib in vitro. Methods: The gefitinib‐resistant RPC‐9 cells were established and the mutations of EGFR were detected by gene sequencing. The ADAM17 shRNA expression vectors were constructed and packaged to recombinant lentivirus. The cell proliferation viability was detected by MTT, and cellular apotosis was analyzed by flow cytometry assay. The expression levels of ADAM17, EGFR and the phosphorylated EGFR were respectively detected by reverse transcription polymerase chain reaction and western blot. TGF‐α production in the supernatant was detected by enzyme‐linked immunosorbent assay. Results: The gefitinib‐resistant RPC‐9 cells in which mutated EGFR (exon 20) carried 790T > T/M mutation were established. When the concentrations of gefitinib were less than 10μmol/L, there were no significant changes in the apoptosis and cellular proliferation of RPC‐9 with the dose‐escalation of gefitinib. The cell proliferation viability of RPC‐9 was significantly decreased by lentivirus mediated ADAM17 RNAi (P 0.05). Gefitinib had no significant effects on TGF alpha production in the supernatants (P > 0.05). Gefitinib did not inhibit EGFR expression in gefitinib‐sensitive PC‐9 and gefitinib‐resistant RPC‐9 cells (P > 0.05). The phosphorylation of EGFR in gefitinib‐sensitive PC‐9 cells was significantly inhibited by gefitinib (P 0.05). Lentivirus mediated ADAM17 RNAi significantly inhibited the mRNA and protein expression of ADAM17 in gefitinib‐resistant RPC‐9 cells (P

Objective: To update the meta-analysis comparing the effectiveness of oral appliance (OA) with continuous positive airway pressure (CPAP) in treating patients with obstructive sleep apnea (...

Liposarcoma is the most common type of soft-tissue sarcoma, and predominantly originates from the extremities and retroperitoneal cavity. However, primary endobronchial liposarcoma is extremely rare. The present study reports on the case of a 54-year-old man, a smoker, diagnosed with primary endobronchial atypical lipomatous tumor/well-differentiated liposarcoma (ALT-WDLS), which was successfully resected via bronchoscopy. Chest computed tomography (CT) revealed a neoplasm in the left main bronchus measuring 12.8×7.8 mm. Bronchoscopy demonstrated multiple roundish, pedunculated, polypoid masses in the left main bronchus. Bioptic specimens were obtained from the roundish masses, and pathological examination revealed an adipose tissue-derived tumor. The masses were completely resected during the second bronchoscopy under general anesthesia. Histopathological examination of the radical resection specimen revealed that it was an ALT-WDLS. The patient showed good quality of life at the 6-month postoperative follow-up without evidence of recurrence. Immunohistochemistry was completed with the human homologue of murine double-minute type 2 (MDM2) (+), cyclin-dependent kinase 4 (CDK4) (+), p16 (+), S-100 (+), Ki-67 (+), cluster of differentiation 34 (CD34) (+) and retinoblastoma protein (+), confirming ALT-WDLS. However, the fluorescence in situ hybridization assay revealed no amplification of MDM2 and CDK4 in the ALT-WDLS. To the best of our knowledge, the present case report is the first to describe the clinicopathologic features and genetic analysis of endobronchial liposarcoma. Although rare, this case is a reminder that clinicians should consider the possibility of this rare endobronchial tumor in patients with nonspecific symptoms including chronic cough, chest pain and recurrent pneumonia. As in this case, endoscopic treatment provided an excellent clinical outcome in patients with primary endobronchial ALT-WDLS.

Secondary resistance is a major limitation in the efficacy of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor treatment of lung cancer. Previous studies have shown that expression of the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is upregulated in lung cancer, which is correlated with metastasis and poor prognosis. However, the precise role of HOTAIR and its effects on gefitinib resistance in human lung adenocarcinoma are not known. To address this issue, in the present study we established a gefitinib-resistant (R)PC-9 human lung adenocarcinoma cell line and examined cell viability with the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. We found that gefitinib concentrations

Heme oxygenase 1 (HMOX1) plays an important role in the development of chronic obstructive pulmonary disease (COPD). However, the association of HMOX1 length polymorphism in promoter region to the risk and severity of COPD has not been well studied. In this study, we searched the databases including PubMed, EMBASE, Cochrane Library and China National Knowledge Infrastructure (CNKI) and extracted the information from related articles. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to study the effect of HMOX1 polymorphism on the risk and severity of COPD. As a result, nine studies were included for this meta‐analysis. Higher frequencies of L allele and type I genotype (containing at least one L allele) were found in patients with COPD (for L allele, OR 2.02, 95% CI: 1.32–3.11, P = 0.001; for type I genotype, OR 1.82, 95% CI: 1.28–2.61, P = 0.001), especially in Asian population (for L allele, OR 2.23, 95% CI: 1.68–2.95, P < 0.001; for type I genotype, OR 2.02, 95% CI: 1.51–2.70, P < 0.001). Genotyping method, source of control subjects, literature quality and language also affected the results to some extent. However, there was little difference in HMOX1 genotypes distribution in patients with COPD with different severity. Our study indicated L allele and type I genotype were related to the susceptibility but not the severity of COPD.

The loss of alveolar structure and airspace enlargement are major pathological changes in chronic obstructive pulmonary disease (COPD). Type II alveolar epithelial cells (AECII) are involved in maintaining lung tissue repair and alveolar homeostasis. Long non‑coding RNAs (lncRNAs) are involved in multi‑regulating gene transcription, affecting processes including embryonic development, cell differentiation and cellular senescence. The primary aim of the present study was to explore the mechanisms of AECII senescence regulated by lncRNA‑mediated sirtuin 1 (SIRT1) and forkhead box O 3a (FoxO3a) signaling pathways in patients with COPD. Lung tissues from patients with COPD exhibited pathological characteristics and significantly increased senescence‑associated β‑galactosidase activity. Furthermore, the expression levels of senescence‑associated lncRNA1 (SAL‑RNA1), SIRT1 and FoxO3a were reduced, but SAL‑RNA2, SAL‑RNA3, p53 and p21 were upregulated in the lung tissues of patients with COPD compared with control. The results of the present study indicated that lncRNA‑mediated SIRT1/p53 and FoxO3a signaling pathways may regulate AECII senescence in the pathogenesis of COPD, which may provide a novel experimental basis for the treatment of COPD.