IL-13 Augments Compressive Stress-Induced Tissue Factor Expression in Human Airway Epithelial Cells Researchers investigated the role of IL-13, a type 2 cytokine, alone and in combination with compressive stress, which mimics asthmatic bronchoconstriction, on tissue factor (TF) expression and release of TF-positive extracellular vesicles from primary normal human bronchial epithelial cells. [Am J Respir Cell Mol Biol] Abstract Posttranscriptional Silencing of the lncRNA MALAT1 by miR-217 Inhibits the Epithelial–Mesenchymal Transition via Enhancer of Zeste Homolog 2 in the Malignant Transformation of HBE Cells Induced by Cigarette Smoke Extract The authors investigated the effects of an miRNA (miR-217) on levels of an lncRNA (MALAT1) and examined the role of these factors in the epithelial–mesenchymal transition induced by cigarette smoke extract in human bronchial epithelial (HBE) cells. [Toxicol Appl Pharmacol] Abstract Continuous Activation of Nrf2 and Its Target Antioxidant Enzymes Leads to Arsenite-Induced Malignant Transformation of Human Bronchial Epithelial Cells By establishing transformed human bronchial epithelial cells via chronic low-dose arsenite treatment, scientists showed that in acquiring this malignant phenotype, continuous low level of ROS and sustained enhancement of nuclear factor-erythroid-2 p45-related factor (Nrf2) and its target antioxidant enzymes levels were observed in the later-stage of arsenite-induced cell transformation. [Toxicol Appl Pharmacol] Abstract Synergistic Proinflammatory Responses by IL-17A and Toll-Like Receptor 3 in Human Airway Epithelial Cells Investigators demonstrated that IL-17A and polyI:C, the ligand of toll-like receptor 3, synergistically induced the expression of proinflammatory cytokines and chemokines, but not type I interferon in primary culture of normal human bronchial epithelial cells. [PLoS One] Full Article Wedelolactone Protects Human Bronchial Epithelial Cell Injury against Cigarette Smoke Extract-Induced Oxidant Stress and Inflammation Responses through Nrf2 Pathway Scientists investigated the effects of wedelolactone (WEL) on normal human bronchial epithelial (NHBE) cell injury induced by cigarette smoke extract (CSE) in vitro. They showed that the pretreatment WEL resulted in a significant protective effect on 10% CSE-induced cell death in NHBE cells. [Int Immunopharmacol] Abstract LUNG CANCER Ursolic Acid Exerts Anti-Cancer Activity by Suppressing Vaccinia-Related Kinase 1-Mediated Damage Repair in Lung Cancer Cells Scientists found that ursolic acid (UA) inhibits the catalytic activity of vaccinia-related kinase 1 (VRK1) via direct binding to the catalytic domain of VRK1. UA weakens surveillance mechanisms by blocking 53BP1 foci formation induced by VRK1 in lung cancer cells, and possesses synergistic anti-cancer effects with DNA damaging drugs. [Sci Rep] Full Article MiR-140-3p Suppressed Cell Growth and Invasion by Downregulating the Expression of ATP8A1 in Non-Small Cell Lung Cancer Researchers identified MicroRNA (miR)-140-3p as a downregulated microRNA in most cancer tissues including lung cancer tissues, compared with their normal counterparts. MiR-140-3p was observed to perform its tumor suppressor function via its inhibition on cell growth, migration and invasion but its induction of cell apoptosis. [Tumour Biol] Abstract The Iron Component of Particulate Matter Is Antiapoptotic: A Clue to the Development of Lung Cancer after Exposure to Atmospheric Pollutants? The authors investigated transition metallic compounds, particularly iron, in order to decipher their underlying molecular mechanisms that prevent apoptosis. Human bronchial epithelial cells were exposed for four hours to different particulate matter samples with established antiapoptotic effect or not or to their metallic components before apoptosis induction by the calcium ionophore A23187 or Staurosporine. [Biochimie] Abstract Placental Growth Factor Promotes Metastases of Non-Small Cell Lung Cancer through MMP9 The authors found that placental growth factor (PLGF) and matrix metalloproteinase 9 (MMP9) levels both significantly increased in the non-small cell lung cancer (NSCLC) specimens and were strongly correlated. Overexpression of PLGF in NSCLC cells increased the levels of MMP9 and cell invasiveness, while inhibition of PLGF in NSCLC cells decreased the levels of MMP9 and cell invasiveness. [Cell Physiol Biochem] Full Article |