• QIANG WANG

      Articles written in Journal of Biosciences

    • MicroRNA-146 protects A549 and H1975 cells from LPS-induced apoptosis and inflammation injury

      QIANG WANG DAGANG LI YUQUAN HAN XIAOQIAN DING TAO XU BINGJIAN TANG

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      Pneumonia is an inflammatory condition affecting the lungs, in which pro-inflammatory cytokines are secreted. It has beenshown that microRNA-146 (miR-146) is involved in the regulation of immune and inflammatory responses. The presentstudy explored the protective effects of miR-146 overexpression on lipopolysaccharide (LPS)-mediated injury in A549 andH1975 cells. In this study, A549 and H1975 cells were transfected with miR-146 mimic or inhibitor, and then weresubjected with LPS. Thereafter, cell viability, colony formation capacity, apoptosis, the release of proinflammatory factors,Sirt1 expression, and the expression of NF-kB and Notch pathway proteins were respectively assessed. As a result, miR-146 overexpression exerted protective functions on LPS-damaged A549 and H1975 cells, as evidenced by the increases incell viability and colony number, the decrease in apoptotic cell rate, as well as the down-regulations of IL-1, IL-6, and TNFa.Sirt1 can be positively regulated by miR-146. Furthermore, miR-146 overexpression blocked NF-kB and Notch pathways,while these blocking effects were abolished when Sirt1 was silenced. The findings in the current study indicated thatmiR-146 protected A549 and H1975 cells from LPS-induced apoptosis and inflammation injury. miR-146 exerted protectivefunctions might be via up-regulation of Sirt1 and thereby blocking NF-kB and Notch pathways.

    • Serum miR-518e-5p is a potential biomarker for secondary imatinib-resistant gastrointestinal stromal tumor

      YOUWEI KOU REN YANG QIANG WANG

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      Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor of the intestinal tract. Imatinib is used asfirst-line therapy for GIST patients; however, secondary imatinib resistance poses a significant clinical challenge. Here, weanalyzed serum miRNA expression profiles to identify specific serum miRNAs that could be used as early diagnosticmarkers. Candidate miRNAs were validated using Taqman quantitative PCR with serum samples from secondary imatinibresistantGIST patients (n = 39), imatinib-sensitive GIST patients (n = 37), and healthy controls (n = 28). Serum miR-518e-5p and miR-548e levels were higher in secondary imatinib-resistant GIST than imatinib-sensitive GIST patients orhealthy controls (P\0.0001). However, ROC analysis indicated that only miR-518e-5p could distinguish imatinibresistantGIST. To discriminate imatinib-resistant from imatinib-sensitive GIST patients, the AUC for serum miR-518e-5pwas 0.9938, with 99.8% sensitivity and 82.1% specificity. Serum miR-518e-5p could also discriminate imatinib-resistantGIST patients from healthy controls with 99.9% sensitivity and 97.4% specificity. These data indicate that serum miR-518e-5p is a potentially promising non-invasive biomarker for early detection and diagnosis of secondary imatinib-resistantGIST.

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