Targeting PI3K-p110α Suppresses Influenza Viral Infection in Chronic Obstructive Pulmonary Disease Scientists characterized the mechanisms of increased susceptibility to influenza virus infection in chronic obstructive pulmonary disease (COPD), and the potential for therapeutic targeting. They utilized a combination of primary bronchial epithelial cells from COPD and healthy control subjects, a mouse model of cigarette smoke-induced experimental COPD and influenza infection. [Am J Respir Crit Care Med] Abstract Imprinting of the COPD Airway Epithelium for Dedifferentiation and Mesenchymal Transition Researchers hypothesized that de-differentiation of the chronic obstructive pulmonary disease (COPD) respiratory epithelium through epithelial-to-mesenchymal transition (EMT) could participate in airway fibrosis and thereby, in airway obstruction. Surgical lung tissue and primary broncho-epithelial cultures from 104 patients were assessed for EMT markers. [Eur Respir J] Abstract Pneumococci LytA-Dependent KLF4 Expression Terminates IL-8 Secretion in Lung Epithelium Scientists tested the hypothesis that Krueppel-like factor 4 (KLF4) may counter-regulate Streptococcus pneumoniae-related human lung epithelial cell activation using the potent pro-inflammatory chemokine interleukin-8 (IL-8) as a model molecule. Pneumococci induced KLF4 expression in human lung, primary human bronchial epithelial cells and the lung-epithelial cell line BEAS-2B. [Am J Respir Cell Mol Biol] Abstract Lactate as Substrate for Mitochondrial Respiration in Alveolar Epithelial Type II Cells Scientists examined lactate utilization by primary alveolar epithelial type II (ATII) cells and the ATII model cell line, MLE-15, and link lactate consumption directly to mitochondrial ATP generation. ATII cells cultured in lactate undergo mitochondrial respiration at near-maximal levels, twice the rates of those grown in glucose, and oxygen consumption under these conditions is directly linked to mitochondrial ATP generation. [Am J Physiol Lung Cell Mol Physiol] Abstract Safranal of Crocus sativus L. Inhibits Inducible Nitric Oxide Synthase and Attenuates Asthma in a Mouse Model of Asthma Researchers evaluated of antioxidant potential of C. sativus and its main constituents, safranal and crocin, in bronchial epithelial cells, followed antiinflammatory potential of the active constituent safranal, in a murine model of asthma. [Phytother Res] Abstract LUNG CANCER ErbB2 Pathway Activation upon Smad4 Loss Promotes Lung Tumor Growth and Metastasis Comparative transcriptomic and in vivo cistromic analyses determined that loss of PTEN and SMAD4 results in ELF3 and ErbB2 pathway activation due to decreased expression of ERRFI1, a negative regulator of ERBB2 in mouse and human cells. [Cell Rep] Full Article | Graphical Abstract Demethoxycurcumin-Carrying Chitosan-Antibody Core-Shell Nanoparticles with Multi-Therapeutic Efficacy toward Malignant A549 Lung Tumor-From In-Vitro Characterization to In-Vivo Evaluation Cell culture experiments using normoxic and multidrug resistant hypoxic cells overexpressing EGFR confirmed improved demethoxycurcumin (DMC) delivery for anti-EGFR coated particles and revealed that the DMC was delivered to the cytoplasmic region of the cells, forming nano-precipitates in lysosomes and endosomes. [Mol Pharm] Abstract The Cystic Fibrosis Transmembrane Conductance Regulator as a Biomarker in Non-Small Cell Lung Cancer Knockdown of cystic fibrosis transmembrane conductance regulator (CFTR) in non-small cell lung cancer cells enhanced malignant behavior; in contrast, overexpression of CFTR suppressed cancer progression in vitro and in vivo. The tumor-suppressing effect of CFTR was associated with inhibition of multiple uPA/uPAR-mediated malignant traits in culture. [Int J Oncol] Abstract Matrine Induces Mitochondrial Apoptosis in Cisplatin-Resistant Non-Small Cell Lung Cancer Cells via Suppression of β-Catenin/Survivin Signaling Investigators determined the cytotoxic effects of matrine on cisplatin-resistant non-small cell lung cancer cells and the associated molecular mechanisms. [Oncol Rep] Abstract |