Utilization of recombinase polymerase amplification method combined with lateral flow dipstick for visual detection of respiratory syncytial virus.

Respiratory syncytial virus (RSV) is a major causative agent of respiratory tract infection necessitating hospitalization in children. A rapid diagnostic method would facilitate early detection of RSV infection and timely implementation of special treatment. Here, a reverse transcription recombinase polymerase amplification (RT-RPA) assay combined with lateral flow dipstick (LFD) was evaluated for rapid visual detection of RSV. The primers were designed to target the conserved L gene. The RT-RPA-LFD assay could simultaneously detect RSV subtype A and B with the same detection limit of 10 copies of a given RNA molecule. Moreover, the assay showed no cross-reactivity with other common human pathogens. The performance of the RT-RPA-LFD assay was evaluated by testing 136 nasopharyngeal aspirates (NPAs). The agreement of the detection results between RT-RPA-LFD and qRT-PCR was 100% (34 positive and 102 negative cases). In summary, the developed RT-RPA-LFD assay had good performance in detecting RSV in clinical specimens, thus providing a novel alternative solution for the detection of RSV under field conditions.

The long noncoding RNA FOXCUT promotes proliferation and migration by targeting FOXC1 in nasopharyngeal carcinoma.

Long noncoding RNAs play an important role in various biological processes, including tumorigenesis. FOXC1 (Forkhead box C1) is a member of the Forkhead box family of transcription factors and plays a crucial role in nasopharyngeal carcinoma. In this study, a novel long noncoding RNA (FOXCUT) located upstream of FOXC1 was investigated in 42 nasopharyngeal carcinoma patients. Our analysis revealed that the expression levels of FOXCUT and FOXC1 in nasopharyngeal carcinoma tissues were significantly higher than those observed in chronic nasopharyngitis tissues and that FOXCUT expression was positively correlated with FOXC1 expression. Additionally, knockdown of FOXCUT significantly inhibited proliferation and migration of nasopharyngeal carcinoma cell lines and resulted in downregulated expression of the matrix metalloproteinase 7 and matrix metalloproteinase 9, as well as vascular endothelial growth factor A and ß-catenin. Our findings suggested that FOXCUT expression contributed to the development and progression of nasopharyngeal carcinoma by targeting FOXC1 and that FOXCUT might be useful as a potential nasopharyngeal carcinoma biomarker and therapeutic target.

Inhibitor of DNA binding 3 reverses cisplatin resistance in human lung adenocarcinoma cells by regulating the PI3K/Akt pathway.

Inhibitor of DNA-binding 3 (ID3) is a helix-loop-helix transcription factor that is associated with cell proliferation, differentiation and drug resistance in human cancer, and with anticancer effects in certain types of cancer cells. The present study investigated whether and how ID3 was involved in multidrug resistance (MDR) in human cisplatin (DDP)-resistant A549/DDP lung adenocarcinoma cells. The underlying mechanism of action was investigated in vitro. Cell Counting Kit-8 (CCK-8) and flow cytometry assays demonstrated that overexpression of ID3 enhanced chemosensitivity and decreased drug efflux in A549/DDP cells. Reverse transcription-quantitative polymerase chain reaction revealed that the expression of anti-apoptotic gene B-cell lymphoma-2 was significantly downregulated in cells expressing exogenous ID3 (P<0.05). These results indicated that ID3 may synergize with DDP to increase apoptosis in A549/DDP cells. ID3 overexpression modulated the activity of phosphoinositide 3-kinase/RAC serine/threonine-protein kinase signaling and downregulated the expression of multi-drug resistance protein-1, indicating that ID3 expression can reverse multi-drug resistance in A549/DDP cells. Collectively, these results indicate that ID3 is a potential effective chemotherapeutic target for the treatment of human DDP-resistant A549 lung adenocarcinoma therapy.

Long noncoding RNA expression profile in fibroblast-like synoviocytes from patients with rheumatoid arthritis.

BACKGROUND: Long noncoding RNAs (lncRNAs) have recently received wide attention as key molecules that mediate a variety of physiological and pathological processes by regulating gene expression; however, knowledge of lncRNAs in rheumatoid arthritis (RA) is limited. Thus, we investigated the lncRNA expression profile in fibroblast-like synoviocytes (FLSs) from patients with RA and explored the function of abundantly expressed lncRNAs. METHODS: LncRNA and mRNA microarrays were performed to identify differentially expressed lncRNAs in RA FLSs compared with normal FLSs. Quantitative polymerase chain reaction (qPCR) was used to validate the results, and correlation analysis was used to analyze the relationship between these aberrantly expressed lncRNAs and clinical characteristics. A receiver operating characteristic (ROC) curve was constructed to evaluate the diagnostic value of the lncRNAs identified. RESULTS: According to the gene expression profiles, 135 lncRNAs were differentially expressed between RA and normal FLSs. Furthermore, qPCR data showed that lncRNA ENST00000483588 was up-regulated and that three lncRNAs (ENST00000438399, uc004afb.1, and ENST00000452247) were down-regulated in RA FLSs. The expression level of ENST00000483588 was positively correlated with the level of C-reactive protein and the Simplified Disease Activity Index score. Moreover, the areas under the ROC curve were 0.85, 0.92, 0.97, and 0.92 for ENST00000483588, ENST00000438399, uc004afb.1, and ENST00000452247, respectively. CONCLUSIONS: The results indicate that the dysregulation of ENST00000483588, ENST00000438399, uc004afb.1, and ENST00000452247 may be involved in the pathological processes of RA and that these lncRNAs may have potential value for the diagnosis and assessment of the disease activity of RA.