Pulmonary fibrosis (PF), characterized by the destruction of lung tissue architecture and the abnormal deposition of extracellular matrix (ECM) proteins, currently has no satisfactory treatment. The role of microRNA (miR)-21 in PF has been reported; the current study attempted to investigate a novel molecular mechanism by which miR-21 exerted its function. Consistent with previous studies, miR-21 inhibition reduced ECM protein levels in bleomycin (BLM)-induced mouse model of PF. In human pulmonary fibroblast (IMR-90), miR-21 inhibition reduced transforming growth factor β1 (TGFβ1)-induced ECM protein expression. Regarding a novel molecular mechanism, TGFβ1 combined with TGFβ1 receptor 1 (TGFβ1RI) to activate SMAD2/3, promote SMAD4 nucleus transformation, and thus regulate miR-21 expression and ECM. SMAD3 and SMADs complex could bind to the promoter region of miR-21 to promote miR-21 expression. In conclusion, miR-21 exerts promotive effects on BLM-induced PF and TGFβ1-induced ECM in IMR-90; TGFβ1 combines with TGFβ1RI to activate SMAD2/3, promote SMAD4 nucleus transformation, promote miR-21 expression, and thus to promote BLM-induced PF and TGFβ1-induced ECM in IMR-90 cells.

Computer tomography-guided transthoracic needle aspiration (CT-TTNA) is a minimally invasive technique for sampling peripheral lung lesions. Radial endobronchial ultrasound-guided transbronchial biopsy (rEBUS-TBB) is an alternative. The present study analyzed and compared rEBUS-TBB and CT-TTNA in the diagnosis of peripheral pulmonary lesions (PPL).Clinical data of 513 patients with PPL who underwent an rEBUS-TBB or CT-TTNA examination were analyzed retrospectively. The positive diagnostic rate, complication rate, and influencing factors of the 2 methods were compared.The positive diagnostic rate and complication rate were significantly higher in CT-TTNA than rEBUS-TBB (P = .001; P < .001, respectively). The rEBUS-TBB group showed a higher positive diagnostic rate in larger lesions (>2 cm) than in smaller (≤2 cm) (P = .012), and was lower in the lesions proximal to the chest wall than those distally located (P = .046); no significant difference was observed in the different pulmonary segments (P = .109). In the CT-TTNA group, the positive diagnostic rate in larger lesions did not differ significantly than the smaller lesions (P = .05); it differed significantly in different segments (P = .044). The incidence of pneumothorax was lower in lesions proximal to the chest wall than those located distally (P = .037). In the rEBUS-TBB group, the success rate of the exploration and biopsy of the lesions was 87.4%; the rate of exploration of larger lesions and with bronchial sign was higher than smaller lesions and without bronchial sign (P < .001; P < .001, respectively) while that of lesions close to the chest wall was lower than those distally located (P = .006).rEBUS-TBB and CT-TTNA are effective and safe in the diagnosis of PPL. The positive diagnostic rate of CT-TTNA is higher than rEBUS-TBB. The incidence of pneumothorax in CT-TTNA is higher than rEBUS-TBB. CT-TTNA is selected for smaller lesions close to the chest wall; rEBUS-TBB is used for lesions larger, distal from the chest wall or with a bronchial sign.

In the present study, the expression of microRNA (miR)-671-3p in non-small-cell lung cancer (NSCLC) was detected via reverse transcription-quantitative polymerase chain reaction analysis, and its role in cell proliferation, apoptosis, migration and invasion was investigated via Cell Counting Kit-8, colony formation, flow cytometry, Transwell and scratch assays, respectively. It was observed that the expression of miR-671-3p was upregulated in NSCLC tissues and cell lines (A549 and H1975). Treatment with miR-671-3p inhibitors suppressed cell proliferation, migration and invasion, and increased apoptosis in vitro, suggesting that miR-671-3p functions as an oncogene in NSCLC. In addition, forkhead box P2 (FOXP2) has been reported to be a tumor suppressor that is downregulated in several types of cancer, and its low expression was confirmed in NSCLC tissues and cell lines in the current study via western blotting. The results of the luciferase reporter assay also demonstrated that miR-671-3p targeted directly the 3′-untranslated region of FOXP2. Furthermore, overexpression of FOXP2 in A549 and H1975 cell lines suppressed the growth, migration and invasion, and promoted apoptosis, whereas these effects were reversed by transfection with miR-671-3p mimics, suggesting that miR-671-3p promoted tumor progression via regulating FOXP2. Taken together, the results reported in the present study implied that miR-671-3p may be a potential therapeutic target in NSCLC.

The pathologic mechanisms of pulmonary fibrosis (PF), one of the most common chronic pulmonary diseases, remain unclear. Napsin A is an aspartic proteinase that has been regarded as a hallmark of pulmonary adenocarcinoma. The present study aimed to investigate the specific function and molecular mechanisms of Napsin A in PF from the perspective of microRNA (miRNA or miR) regulation. In the present study, it was found that miR-1290 downregulated the expression of Napsin A by binding to its 3'-UTR. Cell viability was examined by MTT assay. The protein levels of α-smooth muscle actin (α-SMA), Collagen I and Napsin A were examined by western blot analysis. The predicted targeting of Napsin A by miR-1290 was validated by luciferase reporter assay. The protein content of α-SMA was examined by immunofluorescence staining. miR-1290 was found to be upregulated in blood samples from patients with PF and in TGF-β1-stimulated A549 cells. miR-1290 was found to directly target Napsin A. miR-1290 overexpression also significantly promoted A549 cell proliferation and increased the protein levels of markers of fibrosis. Napsin A knockdown exerted effects on A549 cell proliferation and TGF-β1-induced fibrosis that were similar to those induced by miR-1290 overexpression; more importantly, Napsin A knockdown significantly reversed the effects of miR-1290 inhibition, indicating that miR-1290 promotes TGF-β1-induced fibrosis by targeting Napsin A. Moreover, TGF-β1-induced CAMP responsive element binding protein 1 (cREB1) overexpression promoted the transcription of miR-1290 in A549 cells. On the whole, the findings of the present study demonstrate that TGF-β1-induced cREB1 overexpression induces the significant upregulation of miR-1290 expression, thus aggravating TGF-β1-induced fibrotic changes in A549 cells via the miR-1290 downstream target, Napsin A.