Long noncoding RNAs have been reported to be essential regulators in several human diseases, including tumorigenesis. A recent report revealed that FLVCR1-AS1 promotes the progression of hepatocellular carcinoma. However, whether FLVCR1-AS1 is involved in lung cancer remains unclear. In this study, we found that the expression of FLVCR1-AS1 was increased in lung cancer tissues according to The Cancer Genome Atlas database. Similarly, FLVCR1-AS1 was significantly upregulated in lung cancer cell lines. Knockdown of FLVCR1-AS1 dramatically reduced the cell proliferation, migration, and invasion of SPCA1 and A549.Mechanistically, we found that the expression levels of CTNNB1, SOX4, CCND1, CCND2, c-MYC, as well as nucleus β-catenin were decreased in lung cancer cells after FLVCR1-AS1 silencing. Thus, FLVCR1-AS1 positively regulates the activation of the Wnt/β-catenin pathway. Overexpression of CTNNB1 reversed the effect of FLVCR1-AS1 knockdown on A549 cells. In sum, FLVCR1-AS1 silencing inhibited the proliferation, migration, and invasion of lung cancer cells by inhibiting the activity of the Wnt/β-catenin signaling pathway. K E Y W O R D SFLVCR1-AS1, invasion, lung cancer, migration, proliferation, Wnt/β-catenin

Introduction: This study aimed to investigate the prevalence, clinical and radiographic features, and antibiotic responses of Mycoplasma pneumoniae (M. pneumoniae) infections in hospitalized adults with community-acquired pneumonia (CAP) in China. Methodology: Serum specimens collected from 189 CAP patients in both acute phase and convalescence were tested for IgG, IgA, and IgM mixed antibodies specific to M. pneumoniae. The clinical and radiographic characteristics and efficacy of three antibiotic regimens were compared between patients with M. pneumoniae infection and those without. Results: Among 189 CAP patients, 88 (46.6%) were positive for M. pneumoniae infection. Compared to the negative patients, patients with M. pneumoniae infection were significantly younger, had higher rates of dry cough, and had white blood cell counts of <10 10 /L, but had less purulent sputum. Radiography further showed more centrilobular nodules, ground-glass opacities, tree-in-bud patterns and thickened bronchovascular bundles, but less pleural effusion and larger tracts of real opacities in patients with M. pneumoniae infections. Among the three regimens used, patients with moxifloxacin required significantly shorter fever abatement, treatment, and hospitalization times than those with azithromycin plus ceftriaxone and ceftriaxone only. Conclusions: M. pneumoniae infection was present in almost half of the CAP population in east China, with some distinct clinical and radiographic features. Moxifloxacin was an effective antibiotic for this infection.

BackgroundThe application of gene-loaded microbubbles (MBs) combined with ultrasound that results in increased delivery efficiency may be an excellent method of gene delivery. This study aimed to discuss the effects of ultrasound-MB-mediated microRNA (miR)-449a on lung cancer (LC) development by targeting Notch1.MethodsInitially, miR-449a expression in LC tissues, paracancerous tissues, LC cell lines, and lung epithelial cells was detected and its association with LC patients’ clinical characteristics was analyzed. The gain-of-function studies were performed to probe the roles of miR-449a and ultrasound-MB-mediated miR-449a in LC progression. Then, RT-qPCR combined with Western blot analysis was applied to verify the levels of miR-449a, Notch1, proliferation- and apoptosis-related proteins. Moreover, xenograft tumors in nude mice were also applied for in vivo experiments.ResultsPoorly expressed miR-449a was observed in LC, and its expression was associated with clinical staging, differentiation and lymph node metastasis of LC patients. Overexpression of miR-449a suppressed LC cell proliferation and promoted G2/M arrest and apoptosis. Ultrasound-MB-mediated miR-449a strengthened inhibitory effects of miR-449a on cell growth and resistance to apoptosis. miR-449a inhibited H1299 cell activity by targeting Notch1.ConclusionOur data supported that miR-449a overexpression inhibited LC cell growth, and ultrasound-MB-mediated miR-449a reinforced the repressive effects of miR-449a on LC progression. This investigation may offer new insight for LC treatment.

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