Long non‐coding RNAs (lncRNAs) have emerged as new and important regulators of pathological processes including tumour development. In this study, we demonstrated that differentiation antagonizing non‐protein coding RNA (DANCR) was up‐regulated in lung adenocarcinoma (ADC) and that the knockdown of DANCR inhibited tumour cell proliferation, migration and invasion and restored cell apoptosis rescued; cotransfection with a miR‐496 inhibitor reversed these effects. Luciferase reporter assays showed that miR‐496 directly modulated DANCR; additionally, we used RNA‐binding protein immunoprecipitation (RIP) and RNA pull‐down assays to further confirm that the suppression of DANCR by miR‐496 was RISC‐dependent. Our study also indicated that mTOR was a target of miR‐496 and that DANCR could modulate the expression levels of mTOR by working as a competing endogenous RNA (ceRNA). Furthermore, the knockdown of DANCR reduced tumour volumes in vivo compared with those of the control group. In conclusion, this study showed that DANCR might be an oncogenic lncRNA that regulates mTOR expression through directly binding to miR‐496. DANCR may be regarded as a biomarker or therapeutic target for ADC.

Background Primary pulmonary invasive mucinous adenocarcinoma is a rare and distinct subtype of lung adenocarcinoma. Case presentation A 72-year-old woman presented with productive cough for two months and fever for six days. Chest computed tomography (CT) showed a mass in the left lower lobe. Sputum culture tested negative for bacteria, but the sequence of Actinomyces meyeri was detected by metagenomic next generation sequencing from the bronchoalveolar lavage fluid. It was considered a pathogenic bacterium as the normalized number of DNA sequencing reads was 10 times higher than the normal level. The patient’s symptoms alleviated quickly, and the chest CT lesion shrank to a third of the original size following treatment with penicillin for two months. However, a repeat chest CT performed after four months of treatment revealed that the lesion had expanded. Positron emission tomography/CT revealed that fluorodeoxyglucose metabolism was increased in the mass with surrounding ground glass density of the left lower lobe. Furthermore, CT-guided percutaneous lung biopsy was performed, and hematoxylin–eosin staining showed columnar tumor cells with abundant mucin in the cytoplasm with a basal nucleus. Finally, the patient was diagnosed with pulmonary invasive mucinous adenocarcinoma and agreed to undergo a thoracoscopic surgery. Conclusions Pulmonary invasive mucinous adenocarcinoma is a subset of lung adenocarcinoma with low incidence rate. The clinical features and CT findings are non-specific. A histopathological diagnosis is of fundamental importance in preventing misdiagnosis.

Lung cancer is the most common and lethal cancer worldwide, especially in developing countries. Non-small cell lung cancer (NSCLC) accounts for 85% of all cases of lung cancer. In aprevious study, the protein expression of ubiquitin conjugating enzyme E2 C (UBE2C/UbcH10) in NSCLC tissues and cells was found to be significantly higher than that in adjacent tissues and normal lung epithelial cells. Further study revealed that the aberrant expression of UbcH10 in NSCLC tumors or cancer cells was caused by inactivation of the post-transcriptional regulation mechanism, and thus microRNAs (miRNAs) may play an important. In the present study, it was demonstrated that the expression of microRNA, hsa-miR661-3p, was downregulated and UbcH10 was upregulated in 12 pairs of NSCLC tumors and three NSCLC cell lines. A reporter gene assay revealed that overexpression of hsa-miR661-3p effectively reduced the activity of luciferase expressed by a vector bearing the 3' untranslated region of UbcH10 mRNA. Ectopic hsa-miR661-3p overexpression mediated by lentiviral infection decreased the expression of UbcH10. Infection of Lv-miR661-3p inhibited cell growth and invasion in A549 and SK-MES-1 cells. Mechanistically, hsa-miR661-3p induced cell cycle G2 arrest through regulation of spindle assembly checkpoint (SAC) function. On the basis of the proposed mechanisms, the objective of the study was to inhibit the proliferation of A549 and SK-MES-1 by expressing hsa-miR661-3p in vivo and in vitro. Collectively, our results indicated that downregulation of hsa-miR661-3p was involved in NSCLC and restoration of hsa-miR661-3p impaired the growth of NSCLC cell lines A549 and SK-MES-1, suggesting that hsa-miR661-3p may be a potential target molecule for the therapy of NSCLC.