Potent Proapoptotic Actions of Dihydroartemisinin in Gemcitabine-Resistant A549 Cells Researchers investigated the proapoptotic mechanisms of dihydroartemisinin in gemcitabine (Gem)-resistant A549 (A549GR) cells. A549GR cells exhibited lower basal antioxidant capacity, higher level of basal reactive oxygen species and intracellular Fe2+ than Gem-sensitive A549 cells. [Cell Signal] Abstract ICAM-1 Targeted Nanogels Loaded with Dexamethasone Alleviate Pulmonary Inflammation Investigators studied the potential of targeted nanogels as a drug delivery platform in vivo to alleviate acute pulmonary inflammation in animal model of lipopolysaccharide-induced lung injury. [PLoS One] Full Article Transcriptome Profile Analysis of Saturated Aliphatic Aldehydes Reveals Carbon Number-Specific Molecules Involved in Pulmonary Toxicity Scientists investigated the transcriptomic responses and identified specific molecular signatures of low-molecular-weight saturated aliphatic aldehydes (LSAAs). To evaluate the change in gene expression levels, A549 human alveolar epithelial cells were exposed to six LSAAs (propanal, butanal, pentanal, hexanal, heptanal, and octanal) for 48 hours. [Chem Res Toxicol] Abstract Blockade of PDE4B Limits Lung Vascular Permeability and Lung Inflammation in LPS-Induced Acute Lung Injury To investigate the mechanism of how PDE4B takes part in inflammatory response and the maintenance of vascular integrity, researchers established the experimental model of acute lung injury in vitro and in vivo. [Biochem Biophys Res Commun] Abstract Peptide Regulation of Gene Expression and Protein Synthesis in Bronchial Epithelium Investigators measured Ki67, Mcl-1, p53, CD79, and NOS-3 protein levels in the 1st, 7th, and 14th passages of bronchoepithelial human embryonic cell cultures. [Lung] Abstract LUNG CANCER Quinacrine Overcomes Resistance to Erlotinib by Inhibiting FACT, Nuclear Factor-kappa B, and Cell Cycle Progression in Non-Small Cell Lung Cancer To test drug combinations that could improve the efficacy of erlotinib, researchers combined erlotinib with quinacrine, which inhibits the FACT (facilitates chromatin transcription) complex that is required for NF-kappaB transcriptional activity. In A549, H1975 and H1993 non-small cell lung cancer cells, this drug combination was highly synergistic, as quantified by Chou-Talalay combination indices, and slowed xenograft tumor growth. [Mol Cancer Ther] Abstract Quantitative Proteomic Approach to Understand Metabolic Adaptation in Non-Small Cell Lung Cancer Investigators carried out the proteomic analysis of two KRAS-mutated non-small cell lung cancer (NSCLC) cell lines and a non-tumoral bronchial cell line using an iTRAQ (isobaric Tags for Relative and Absolute Quantitation) approach combined with two-dimensional fractionation and MALDI-TOF/TOF mass spectrometry analysis. [J Proteome Res] Abstract Evidence that RASSF1C Stimulation of Lung Cancer Cell Proliferation Depends on IGFBP-5 and PIWIL1 Expression Levels The authors report that RASSF1C promotes lung cancer cell migration and enhances lung cancer cell tumor sphere formation. They also show that RASSF1C over-expression reduces the inhibitory effects of the anti-cancer agent, betulinic acid, on lung cancer cell proliferation. [PLoS One] Full Article TNF-Related Apoptosis-Inducing Ligand Enhances Vinorelbine-Induced Apoptosis and Antitumor Activity in a Preclinical Model of Non-Small Cell Lung Cancer The authors evaluated the antitumor effects of the two drugs (TRAIL and NVB alone or in combination) by inducing apoptosis in vitro and in vivo. Using the human non-small cell lung cancer cell line and a BALB/c nude mice model, they observed the cell viability, cell apoptosis and cell proliferation. [Oncol Rep] Abstract MicroRNA-1290 Promotes Asiatic Acid-Induced Apoptosis by Decreasing BCL2 Protein Level in A549 Non-Small Cell Lung Carcinoma Cells Investigators identified an important regulator of asiatic acid-induced cell death, microRNA-1290, which sensitizes cells to asiatic acid-induced cytotoxicity and negatively regulates BCL2 expression. [Oncol Rep] Abstract |