Pulmonary Cell News Volume 4.16 | Apr 30 2015

Deleterious Impact of Hyperglycemia on Cystic Fibrosis Airway Ion Transport and Epithelial Repair
Scientists evaluated the impact of hyperglycemia on airway epithelial repair and transepithelial ion transport, which are critical in maintaining lung integrity and function. Non-cystic fibrosis (CF) and CF airway epithelial cells were exposed to low or high glucose before ion current and wound repair rate measurements. [J Cyst Fibros] Abstract

Glucocorticoids Distinctively Modulate the CFTR Channel with Possible Implications in Lung Development and Transition into Extrauterine Life
Researchers analyzed the influence of glucocorticoids on pulmonary Cl^– channels. Alveolar cells from fetal and adult rats, A549 cells, bronchial Calu-3 and 16HBE14o- cells, and primary rat airway cells were studied with real-time quantitative PCR and Ussing chambers. [PLoS One] Full Article

Effect of Elevated Carbon Dioxide on Bronchial Epithelial Innate Immune Receptor Response to Organic Dust from Swine Confinement Barns
Innate immune responses to Pam3CSK4, LPS and a complex innate immune stimulus, an extract from the organic dust of swine confinement barns, were tested in a human bronchial epithelial cell line, BEAS-2B. [Int Immunopharmacol] Abstract

LUNG CANCER

FLLL12 Induces Apoptosis in Lung Cancer Cells through a p53/p73-Independent but Death Receptor 5-Dependent Pathway
Scientists investigated the mechanism of anti-tumor effect of FLLL12 in lung cancers. IC₅₀ values measured by sulforhodamine B assay at 72 hours and apoptosis assays suggest that FLLL12 is 5-10–fold more potent than curcumin against a panel of premalignant and malignant lung cancer cell lines, depending on the cell line. [Cancer Lett] Abstract

PNAS-4, an Early DNA Damage Response Gene, Induces S Phase Arrest and Apoptosis by Activating Checkpoint Kinases in Lung Cancer Cells
Scientists found that PNAS-4 expression in lung tumor tissues is significantly lower than that in adjacent lung tissues and its expression is significantly increased in A549 cells after exposure to cisplatin, methyl methane sulfonate and mitomycin, and that its overexpression induces S-phase arrest and apoptosis in lung cancer cells, leading to proliferation inhibition irrespective of their p53 status. [J Biol Chem] Abstract | Full Article

miR-205 and miR-218 Expression Is Associated with Carboplatin Chemoresistance and Regulation of Apoptosis via Mcl-1 and Survivin in Lung Cancer Cells
The authors investigated the role of two distinct miR members, the miR-205 and the tumor suppressor miR-218 in the proliferation, invasion and induction of apoptosis in lung cancer cells after carboplatin treatment. [Cell Signal] Abstract

High EMT Signature Score of Invasive Non-Small Cell Lung Cancer (NSCLC) Cells Correlates with NFκB Driven Colony-Stimulating Factor 2 (CSF2/GM-CSF) Secretion by Neighboring Stromal Fibroblasts
Researchers established co-cultures of invasive or non-invasive NSCLC cell lines and various types of fibroblasts to more precisely characterize the molecular mechanism of tumor-stroma crosstalk in lung cancer. [PLoS One] Full Article

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OncoGenex Announces Custirsen Phase III “ENSPIRIT” Trial Update
OncoGenex Pharmaceuticals, Inc. announced it has filed an amendment with the U.S. Food and Drug Administration, as well as initiated filing with regulatory agencies in other countries, to amend the statistical design and analysis plan of its pivotal, international Phase III ENSPIRIT trial evaluating custirsen in the treatment of non-small cell lung cancer (NSCLC). [OncoGenex Pharmaceuticals, Inc.] Press Release

UAB Secures $11 Million DOD Grant for COPD Study
Researchers at the University of Alabama at Birmingham (UAB) will lead a multisite study of the role of beta blockers in patients with chronic obstructive pulmonary disease, or COPD. The study is funded by an $11 million grant from the United States Department of Defense (DOD). [University of Alabama at Birmingham] Press Release

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Scientist – Pluripotent Stem Cell Biology Endoderm Lineages (STEMCELL Technologies Inc.)

Postdoctoral Research Position – Lung Cancer (University of California, San Francicso)

PhD Student – Molecular Biology and Medicine of the Lung (Philipps-Universität Marburg)

Professorship – Lung Epithelial Cell Plasticity (Ludwig-Maximilians-Universitat München)

PhD Position – Development of a 3D In Vitro Model of Infected Airway (Helmholtz Centre for Infection Research)

PhD Studentship – Cystic Fibrosis (University of East Anglia)

Postdoctoral Researcher – Pulmonary Developmental Pathology (Drexel University College of Medicine)

Postdoctoral Position – Airway Disease and Inflammation (Brigham and Women’s Hospital Harvard Medical School)

Postdoctoral Scholar – Molecular Mechanisms of Lung Cancer, Lung Regeneration and Lung Development (University of California, San Francisco)

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