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Background Long non-coding RNAs (lncRNAs) have been uncovered to be essential regulators in the biological processes of human cancers, including lung adenocarcinoma (LUAD). Recently, small nucleolar RNA host gene 17 (SNHG17) has been identified as one novel oncogenic lncRNA in gastric cancer. However, it remains unclear whether SNHG7 exert functions in LUAD progression. Methods The expression levels of SNHG17, miR-485–5p and Wnt ligand secretion mediator (WLS) in LUAD cells was evaluated by RT-qPCR. The effect of SNHG7 silencing on LUAD cell proliferation was assessed by colony formation and EdU assays. The apoptosis of LUAD cells was measured by flow cytometry analysis. Transwell assays were applied to detect cell migration and invasion. The relationship between SNHG17 and miR-485–5p was validated by RIP, RNA pull down and luciferase reporter assays. Results SNHG17 and WLS were up-regulated in LUAD cell lines. Down-regulation of SNHG17 curbed LUAD cell proliferation, migration and invasion but facilitated apoptosis. SNHG17 acted as miR-485–5p sponge to upregulate WLS expression. Conclusion SNHG17 triggers the progression of LUAD via sponging miR-485–5p to upregulate WLS expression.

Purpose LINC00680 was reported to be involved in various cancers through multiple mechanisms. Therefore, we intended to investigate its role in the progression of non-small cell lung cancer (NSCLC). Materials and methods Firstly, quantitative real-time polymerase chain reaction (qRT-PCR) was used to test LINC00680 in NSCLC tissue and cell lines. Subsequently, A549 and H1299 cells were transfected with LINC00680 overexpressing plasmids and their proliferation and colony formation and apoptosis was tested by Transwell assay and flow cytometry. In addition, xenograft tumor experiments in nude mice also affirmed. Meanwhile, we predicted that miR-410-3p, LINC00680 and high-mobility group protein box 1(HMGB1) relationship by Starbase, dual-luciferase reporter and RIP assay. Finally, the carcinogenic effects of LINC00680 were reversed by ethyl pyruvate (EP), a specific inhibitor of HMGB1. Results LINC00680 was upregulated in NSCLC and was closely related to the malignancy and poor prognosis of NSCLC patients. LINC00680 promoted proliferation and colony formation and inhibited apoptosis of A549 and H1299 cells. In addition, overexpressing LINC00680 accelerated the growth of NSCLC cells in xenograft tumor experiments in nude mice also affirmed. Meanwhile, high-mobility group protein box 1(HMGB1) was astoundingly amplified in NSCLC and was negatively regulated by miR-410-3p. Further, HMGB1 acted as a downstream target of miR-410-3p, upregulating miR-410-3p to attenuate HMGB1, while LINC00680 strengthened the expression of HMGB1 in A549 and H1299 cells. Discussion Thus, these results indicated that LINC00680 was cancerogenic in NSCLC by upregulating HMGB1 via sponging miR-410-3p.

Circular RNAs (circRNAs) have recently been described as key regulators in the progression of non-small cell lung cancer (NSCLC), and this study aimed to investigate the functional role of circMAT2B in NSCLC. CircMAT2B expression in NSCLC tissues and cell lines was investigated using RT-qPCR analysis. A series of functional experiments, including MTT assay, colony formation assay, wound healing assay and transwell assay, were carried out to investigate the effects of circMAT2B knockdown/overexpression on the malignant traits of NSCLC cells. Western blot analysis was performed to detect the expression of EMT-related proteins. Dual-luciferase reporter assay and RIP assay were further carried out to analyze the interaction between circMAT2B and miR-431 in NSCLC. We observed that circMAT2B was overexpressed in NSCLC tissues and cell lines, and high expression of circMAT2B was closely associated with large tumor size, advanced TNM stage and poor prognosis of NSCLC patients. Further functional experiments showed that circMAT2B knockdown markedly inhibited the proliferation, migration, invasion and EMT of NSCLC cells, whereas circMAT2B overexpression led to the opposing results. Mechanistically, circMAT2B could directly interact with miR-431, and subsequently decrease miR-431 expression in NSCLC. The effects of circMAT2B overexpression in NSCLC cells were abrogated by miR-431 restoration. Our findings revealed the novel oncogenic roles of circMAT2B in NSCLC by sponging miR-431.

Primary pulmonary lymphoepithelioma-like carcinoma (PPLELC) is a rare subtype of non-small cell lung cancer (NSCLC) for which there is currently no recognized treatment. Recently, favorable immune checkpoint blockade responses have been observed in PPLELC. This study aimed to review the effects of this regimen in patients with advanced PPLELC. PPLELC patients treated with immune checkpoint inhibitors at West China Hospital between January 2008 and December 2019 were retrospectively identified. Demographic parameters and antitumor treatment details were retrieved and reviewed. Among 128 patients diagnosed with PPLELC, 5 who received immune checkpoint inhibitors at advanced stages were included in the analysis. All of these patients were female nonsmokers with a median age of 55.6 (range 53-58) years at diagnosis. Their median PD-L1 expression was 40% (range, 30-80%). Although the patients underwent surgeries, chemotherapy and radiotherapy, all the treatments failed. Immune checkpoint inhibitors were administered palliatively, and three patients responded favorably, with the best overall response being partial remission (PR). Thus, immune checkpoint inhibitors may be a promising treatment for advanced PPLELC, and large clinical trials are warranted to obtain more evidence regarding this regimen.

Lung cancer is the leading cause of cancer death and there have been clinical prediction models. This study aimed to evaluate the diagnostic performance of published models and create new models to evaluate the probability of malignant solitary pulmonary nodules (SPNs) in Chinese population. We consecutively enrolled 2061 patients with SPNs from West China Hospital between January 2008 and December 2016, each SPN was pathologically confirmed. First, four published prediction models, Mayo clinic model, Veterans Affairs (VA) model, Brock model and People’s Hospital of Peking University (PEH) model were validated in our patients. Then, utilizing logistic regression, decision tree and random forest (RF), we developed three new models and internally validated them. Area under the receiver operating characteristic curve (AUC) values of four published models were as follows: Mayo 0.705 (95% CI 0.658–0.752, n = 726), VA 0.64 6 (95% CI 0.598–0.695, n = 800), Brock 0.575 (95% CI 0.502–0.648, n = 550) and PEH 0.675 (95% CI 0.627–0.723, n = 726). Logistic regression model, decision tree model and RF model were developed, AUC values of these models were 0.842 (95% CI 0.778–0.906), 0.734 (95% CI 0.647–0.821), 0.851 (95% CI 0.789–0.914), respectively. The four published lung cancer prediction models do not apply to our population, and we have established new models that can be used to predict the probability of malignant SPNs.

Dasatinib is a tyrosine kinase inhibitor for the treatment of BCR-ABL-positive chronic myeloid leukaemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukaemia (ALL). Although fluid retention is a common adverse event associated with dasatinib, chylothorax is exceptionally rare. The pathological mechanism, clinical manifestation and management of dasatinib-induced chylothorax are completely unclear. A 71-year-old man treated with dasatinib for CML was admitted for progressive dyspnea. Computed tomography (CT) showed a pleural effusion that was more prominent on the right thoracic cavity. Thoracentesis showed thick milky pleural fluid, which was then confirmed as chylothorax by chylum qualitative tests and triglyceride measurements. Radionuclide lymphoscintigraphy yielded an obstruction at the end segment of the thoracic duct, but no leakage points were found. After excluding common causes, drug-induced chylothorax was presumed. Then, dasatinib was withdrawn, and 1 week later, chylothorax resolved. To further elucidate the relationship between the medication and chylothorax, dasatinib was resumed tentatively for 2 days. As expected, pleural effusion recurred soon. Based on these clinical manifestations, the diagnosis of dasatinib-induced chylothorax was identified. The patient was suggested to stop dasatinib and use an alternative drug as recommended by the haematologist. Pleural effusion is the common adverse reaction of dasatinib, but chylothorax is rare. Only six cases of dasatinib-induced chylothorax have been reported, and our patient is the seventh case. Once a patient with dasatinib treatment develops chylothorax, dasatinib should be considered one of the possible causes. If no other definitive aetiological factor is identified, dasatinib discontinuation might be the optimum scheme.

Background This meta-analysis aimed to systematically estimate the prevalence of comorbid bronchiectasis in patients with asthma and to summarize its clinical impact. Methods Embase, PubMed, and Cochrane Library electronic databases were searched to identify relevant studies published from inception until March 2020. Study selection Studies were included if bronchiectasis was identified by high-resolution computed tomography. Outcomes included the prevalence of bronchiectasis and its association with demographic characteristics and indicators of asthma severity, including results of lung function tests and the number of exacerbations. Results Five observational studies with 839 patients were included. Overall, the mean prevalence of bronchiectasis in patients with asthma was 36.6% (307/839). Patients with comorbid bronchiectasis had lower forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) (MD: -2.71; 95% CI: -3.72 to -1.69) and more frequent exacerbations (MD: 0.68; 95% CI: 0.03 to 1.33) than those with asthma alone, and there was no significant difference of sex, duration of asthma and serum levels of immunoglobulin(Ig)Es between asthmatic patients with or without bronchiectasis. Conclusion The presence of bronchiectasis in patients with asthma was associated with greater asthma severity. There are important therapeutic implications of identifying bronchiectasis in asthmatic patients.

Adenoid cystic carcinoma (ACC) is the second most common tracheal tumor, but its optimal treatment strategy is still controversial. To further elucidate the impact of treatment on disease-free survival (DFS) and overall survival (OS), we retrospectively investigated different treatment modalities and outcomes of 56 patients with primary ACC of the trachea treated at four hospitals in Sichuan Province of China from 1995 to 2012. 52 patients were included in the analysis. 4 patients with unresectable tumors were treated primarily with radiotherapy (RT) alone. 11 of 48 patients who received surgery as primary therapy obtained complete resection without adjuvant therapy. 24 of 37 patients who had incomplete resection (R1, R2) received postoperative RT while 13 patients were treated without postoperative RT. Postoperative chemotherapy (CT) was used in 12 patients with postoperative RT. No significant difference was shown in DFS (p = 0.683) and OS (p = 0.829) between patients with complete resection and those with incomplete resection. Postoperative RT for patients with incomplete resection was associated with improved DFS (92 vs. 62 months, p = 0.027) and OS (125 vs. 78 months, p = 0.004). Postoperative chemotherapy (CT) following RT did not have a significant impact on DFS (p = 0.390) or OS (p = 0.646) in patients with positive margin. These observations suggest that postoperative RT should probably be recommended for patients with incomplete resection. Postoperative CT following RT in patients with incomplete resection did not seem to produce an additional survival benefit.

A number of polymorphisms in a disintegrin and metalloprotease 33 (ADAM33) gene have been implicated in susceptibility to chronic obstructive pulmonary disease (COPD). However, results to date have been inconclusive. We conducted meta-analyses to investigate the associations between multiple polymorphisms in ADAM33 gene and COPD susceptibility. PubMed, Embase and Chinese databases (Wanfang and China National Knowledge Infrastructure) were searched for eligible case-control studies. We extracted data and used meta-analysis to calculate pooled odds ratios with 95% confidence intervals to evaluate the strength of associations. Twelve studies containing six ADAM33 polymorphisms (F+1, S1, S2, T1, V4 and Q-1) were identified, which involved 2630 cases and 4376 controls. ADAM33 S1 polymorphism showed stable and significant associations with COPD risks among the Chinese and smoking populations, and Q-1 polymorphism showed stable and significant associations with COPD risks among the overall populations. In subgroup analyses, T1 and Q-1 polymorphisms were significantly associated with COPD risks among the Chinese and smoking populations, and among the Chinese, Caucasians and smoking populations, respectively. However, none of the significant results was stable in sensitivity analyses. With respect to F+1, S2 or V4 polymorphism, there was no evidence of any significant association with COPD risks in either the overall or the subgroup analysis. The results of this meta-analysis indicate that ADAM33 S1 polymorphism is a risk factor for COPD among the Chinese and smoking populations, and that Q-1 polymorphism is a risk factor for COPD among the overall populations.