miR-135a Inhibits Non-Small Cell Lung Cancer Progression by Suppressing RAB1B Expression and the RAS Pathway

Researchers showed that miR-135a was aberrantly downregulated in non-small cell lung cancer (NSCLC) cells in comparison with normal bronchial epithelial cells, and the expression of miR-135a inhibited proliferation, invasion and metastasis of NSCLC cells in vitro.
[Aging]
Aging | MiR-135a inhibits non-small cell lung cancer progression by suppressing RAB1B expression and the RAS pathway - Full Text. (n.d.). Retrieved July 31, 2020, from https://www.aging-us.com/article/103494/text Cite
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IL-17A-Producing T Cells Exacerbate Fine Particulate Matter-Induced Lung Inflammation and Fibrosis by Inhibiting PI3K/Akt/mTOR-Mediated Autophagy

Primary bronchial epithelial cells (mBECs) were extracted, and the expression of TGF signaling pathway‐, autophagy‐ and PI3K/Akt/mTOR signaling pathway‐related proteins in mBECs was detected by immunofluorescence assay and Western blot analysis.
[Journal of Cellular and Molecular Medicine]
Cong, L.-H., Li, T., Wang, H., Wu, Y.-N., Wang, S.-P., Zhao, Y.-Y., … Duan, J. (n.d.). IL-17A-producing T cells exacerbate fine particulate matter-induced lung inflammation and fibrosis by inhibiting PI3K/Akt/mTOR-mediated autophagy. Journal of Cellular and Molecular Medicine, n/a(n/a). https://doi.org/10.1111/jcmm.15475 Cite
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Indium Oxide Nanoparticles Induce Lung Intercellular Toxicity between Bronchial Epithelial Cells and Macrophages

The effects of indium oxide nanoparticles on lung cells associated with respiratory and immune barriers and the toxic effects of intercellular cascades were studied.
[Journal of Applied Toxicology]
Indium oxide nanoparticles induce lung intercellular toxicity between bronchial epithelial cells and macrophages - Li - - Journal of Applied Toxicology - Wiley Online Library. (n.d.). Retrieved July 2, 2020, from https://onlinelibrary.wiley.com/doi/abs/10.1002/jat.4023 Cite
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PEBP1 Acts as a Rheostat between Prosurvival Autophagy and Ferroptotic Death in Asthmatic Epithelial Cells

The concomitant activation of ferroptosis and autophagy by 15-lipoxygenase-1–PE-binding protein-1 complexes and their hydroperoxy-phospholipids revealed a pathobiologic pathway relevant to asthma and amenable to therapeutic targeting.
[Proceedings of the National Academy of Sciences of the United States of America]
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Antisense Oligonucleotide-Mediated Correction of CFTR Splicing Improves Chloride Secretion in Cystic Fibrosis Patient-Derived Bronchial Epithelial Cells

Researchers tested an antisense oligonucleotide targeting the cystic fibrosis (CF) transmembrane conductance regulator c.3718-2477C>T mutation and showed that it effectively blocks aberrant splicing in primary bronchial epithelial cells from CF patients with the mutation.
[Nucleic Acids Research]
Michaels, W. E., Bridges, R. J., & Hastings, M. L. (n.d.). Antisense oligonucleotide-mediated correction of CFTR splicing improves chloride secretion in cystic fibrosis patient-derived bronchial epithelial cells. Nucleic Acids Research. https://doi.org/10.1093/nar/gkaa490 Cite
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